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Ageing – Wikipedia

08-12-2016 9:43 am

Ageing, also spelled aging, is the process of becoming older. The term refers especially to human beings, many animals, and fungi, whereas for example bacteria, perennial plants and some simple animals are potentially immortal. In the broader sense, ageing can refer to single cells within an organism which have ceased dividing (cellular senescence) or to the population of a species (population ageing).

In humans, ageing represents the accumulation of changes in a human being over time,[1] encompassing physical, psychological, and social change. Reaction time, for example, may slow with age, while knowledge of world events and wisdom may expand. Ageing is among the greatest known risk factors for most human diseases:[2] of the roughly 150,000 people who die each day across the globe, about two thirds die from age-related causes.

The causes of ageing are unknown; current theories are assigned to the damage concept, whereby the accumulation of damage (such as DNA breaks, oxidised DNA and/or mitochondrial malfunctions)[3] may cause biological systems to fail, or to the programmed ageing concept, whereby internal processes (such as DNA telomere shortening) may cause ageing. Programmed ageing should not be confused with programmed cell death (apoptosis).

The discovery, in 1934, that calorie restriction can extend lifespan by 50% in rats has motivated research into delaying and preventing ageing.

Human beings and members of other species, especially animals, necessarily experience ageing and mortality. Fungi, too, can age.[4] In contrast, many species can be considered immortal: for example, bacteria fission to produce daughter cells, strawberry plants grow runners to produce clones of themselves, and animals in the genus Hydra have a regenerative ability with which they avoid dying of old age.

Early life forms on Earth, starting at least 3.7 billion years ago,[5] were single-celled organisms. Such single-celled organisms (prokaryotes, protozoans, algae) multiply by fissioning into daughter cells, thus do not age and are innately immortal.[6][7]

Ageing and mortality of the individual organism became possible with the evolution of sexual reproduction,[8] which occurred with the emergence of the fungal/animal kingdoms approximately a billion years ago, and with the evolution of flowering plants 160 million years ago. The sexual organism could henceforth pass on some of its genetic material to produce new individuals and itself could become disposable with regards to the survival of its species.[8] This classic biological idea has however been perturbed recently by the discovery that the bacterium E. coli may split into distinguishable daughter cells, which opens the theoretical possibility of “age classes” among bacteria.[9]

Even within humans and other mortal species, there are cells with the potential for immortality: cancer cells which have lost the ability to die when maintained in cell culture such as the HeLa cell line,[10] and specific stem cells such as germ cells (producing ova and spermatozoa).[11] In artificial cloning, adult cells can be rejuvenated back to embryonic status and then used to grow a new tissue or animal without ageing.[12] Normal human cells however die after about 50 cell divisions in laboratory culture (the Hayflick Limit, discovered by Leonard Hayflick in 1961).[10]

A number of characteristic ageing symptoms are experienced by a majority or by a significant proportion of humans during their lifetimes.

Dementia becomes more common with age.[35] About 3% of people between the ages of 6574 have dementia, 19% between 75 and 84 and nearly half of those over 85 years of age.[36] The spectrum includes mild cognitive impairment and the neurodegenerative diseases of Alzheimer’s disease, cerebrovascular disease, Parkinson’s disease and Lou Gehrig’s disease. Furthermore, many types of memory may decline with ageing, but not semantic memory or general knowledge such as vocabulary definitions, which typically increases or remains steady until late adulthood[37] (see Ageing brain). Intelligence may decline with age, though the rate may vary depending on the type and may in fact remain steady throughout most of the lifespan, dropping suddenly only as people near the end of their lives. Individual variations in rate of cognitive decline may therefore be explained in terms of people having different lengths of life.[38] There might be changes to the brain: after 20 years of age there may be a 10% reduction each decade in the total length of the brain’s myelinated axons.[39][40]

Age can result in visual impairment, whereby non-verbal communication is reduced,[41] which can lead to isolation and possible depression. Macular degeneration causes vision loss and increases with age, affecting nearly 12% of those above the age of 80.[42] This degeneration is caused by systemic changes in the circulation of waste products and by growth of abnormal vessels around the retina.[43]

A distinction can be made between “proximal ageing” (age-based effects that come about because of factors in the recent past) and “distal ageing” (age-based differences that can be traced back to a cause early in person’s life, such as childhood poliomyelitis).[38]

Ageing is among the greatest known risk factors for most human diseases.[2] Of the roughly 150,000 people who die each day across the globe, about two thirds100,000 per daydie from age-related causes. In industrialised nations, the proportion is higher, reaching 90%.[44][45][46]

At present, researchers are only just beginning to understand the biological basis of ageing even in relatively simple and short-lived organisms such as yeast.[47] Less still is known about mammalian ageing, in part due to the much longer lives in even small mammals such as the mouse (around 3 years). A primary model organism for studying ageing is the nematode C. elegans, thanks to its short lifespan of 23 weeks, the ability to easily perform genetic manipulations or suppress gene activity with RNA interference, and other factors.[48] Most known mutations and RNA interference targets that extend lifespan were first discovered in C. elegans.[49]

Factors that are proposed to influence biological ageing[50] fall into two main categories, programmed and damage-related. Programmed factors follow a biological timetable, perhaps a continuation of the one that regulates childhood growth and development. This regulation would depend on changes in gene expression that affect the systems responsible for maintenance, repair and defence responses. Damage-related factors include internal and environmental assaults to living organisms that induce cumulative damage at various levels.[51]

There are three main metabolic pathways which can influence the rate of ageing:

It is likely that most of these pathways affect ageing separately, because targeting them simultaneously leads to additive increases in lifespan.[53]

The rate of ageing varies substantially across different species, and this, to a large extent, is genetically based. For example, numerous perennial plants ranging from strawberries and potatoes to willow trees typically produce clones of themselves by vegetative reproduction and are thus potentially immortal, while annual plants such as wheat and watermelons die each year and reproduce by sexual reproduction. In 2008 it was discovered that inactivation of only two genes in the annual plant Arabidopsis thaliana leads to its conversion into a potentially immortal perennial plant.[54]

Clonal immortality apart, there are certain species whose individual lifespans stand out among Earth’s life-forms, including the bristlecone pine at 5062 years[55] (however Hayflick states that the bristlecone pine has no cells older than 30 years), invertebrates like the hard clam (known as quahog in New England) at 508 years,[56] the Greenland shark at 400 years,[57] fish like the sturgeon and the rockfish, and the sea anemone[58] and lobster.[59][60] Such organisms are sometimes said to exhibit negligible senescence.[61] The genetic aspect has also been demonstrated in studies of human centenarians.

In laboratory settings, researchers have demonstrated that selected alterations in specific genes can extend lifespan quite substantially in yeast and roundworms, less so in fruit flies and less again in mice. Some of the targeted genes have homologues across species and in some cases have been associated with human longevity.[62]

Caloric restriction substantially affects lifespan in many animals, including the ability to delay or prevent many age-related diseases.[103] Typically, this involves caloric intake of 6070% of what an ad libitum animal would consume, while still maintaining proper nutrient intake.[103] In rodents, this has been shown to increase lifespan by up to 50%;[104] similar effects occur for yeast and Drosophila.[103] No lifespan data exist for humans on a calorie-restricted diet,[76] but several reports support protection from age-related diseases.[105][106] Two major ongoing studies on rhesus monkeys initially revealed disparate results; while one study, by the University of Wisconsin, showed that caloric restriction does extend lifespan,[107] the second study, by the National Institute on Ageing (NIA), found no effects of caloric restriction on longevity.[108] Both studies nevertheless showed improvement in a number of health parameters. Notwithstanding the similarly low calorie intake, the diet composition differed between the two studies (notably a high sucrose content in the Wisconsin study), and the monkeys have different origins (India, China), initially suggesting that genetics and dietary composition, not merely a decrease in calories, are factors in longevity.[76] However, in a comparative analysis in 2014, the Wisconsin researchers found that the allegedly non-starved NIA control monkeys in fact are moderately underweight when compared with other monkey populations, and argued this was due to the NIA’s apportioned feeding protocol in contrast to Wisconsin’s truly unrestricted ad libitum feeding protocol.[109] They conclude that moderate calorie restriction rather than extreme calorie restriction is sufficient to produce the observed health and longevity benefits in the studied rhesus monkeys.[110]

In his book How and Why We Age, Hayflick says that caloric restriction may not be effective in humans, citing data from the Baltimore Longitudinal Study of Aging which shows that being thin does not favour longevity.[need quotation to verify][111] Similarly, it is sometimes claimed that moderate obesity in later life may improve survival, but newer research has identified confounding factors such as weight loss due to terminal disease. Once these factors are accounted for, the optimal body weight above age 65 corresponds to a leaner body mass index of 23 to 27.[112]

Alternatively, the benefits of dietary restriction can also be found by changing the macro nutrient profile to reduce protein intake without any changes to calorie level, resulting in similar increases in longevity.[113][114] Dietary protein restriction not only inhibits mTOR activity but also IGF-1, two mechanisms implicated in ageing.[74] Specifically, reducing leucine intake is sufficient to inhibit mTOR activity, achievable through reducing animal food consumption.[115][116]

The Mediterranean diet is credited with lowering the risk of heart disease and early death.[117][118] The major contributors to mortality risk reduction appear to be a higher consumption of vegetables, fish, fruits, nuts and monounsaturated fatty acids, i.e., olive oil.[119]

The amount of sleep has an impact on mortality. People who live the longest report sleeping for six to seven hours each night.[120][121] Lack of sleep (9 hours) is associated with a doubling of the risk of death, though not primarily from cardiovascular disease.[122] Sleeping more than 7 to 8 hours per day has been consistently associated with increased mortality, though the cause is probably other factors such as depression and socioeconomic status, which would correlate statistically.[123] Sleep monitoring of hunter-gatherer tribes from Africa and from South America has shown similar sleep patterns across continents: their average sleeping duration is 6.4 hours (with a summer/winter difference of 1 hour), afternoon naps (siestas) are uncommon, and insomnia is very rare (tenfold less than in industrial societies).[124]

Physical exercise may increase life expectancy.[125] People who participate in moderate to high levels of physical exercise have a lower mortality rate compared to individuals who are not physically active.[126] Moderate levels of exercise have been correlated with preventing aging and improving quality of life by reducing inflammatory potential.[127] The majority of the benefits from exercise are achieved with around 3500 metabolic equivalent (MET) minutes per week.[128] For example, climbing stairs 10 minutes, vacuuming 15 minutes, gardening 20 minutes, running 20 minutes, and walking or bicycling for 25 minutes on a daily basis would together achieve about 3000 MET minutes a week.[128]

Avoidance of chronic stress (as opposed to acute stress) is associated with a slower loss of telomeres in most but not all studies,[129][130] and with decreased cortisol levels. A chronically high cortisol level compromises the immune system, causes cardiac damage/arterosclerosis and is associated with facial ageing, and the latter in turn is a marker for increased morbidity and mortality.[131][132] Stress can be countered by social connection, spirituality, and (for men more clearly than for women) married life, all of which are associated with longevity.[133][134][135]

The following drugs and interventions have been shown to retard or reverse the biological effects of ageing in animal models, but none has yet been proven to do so in humans.

Evidence in both animals and humans suggests that resveratrol may be a caloric restriction mimetic.[136]

As of 2015 metformin was under study for its potential effect on slowing ageing in the worm C.elegans and the cricket.[137] Its effect on otherwise healthy humans is unknown.[137]

Rapamycin was first shown to extend lifespan in eukaryotes in 2006 by Powers et al. who showed a dose-responsive effect of rapamycin on lifespan extension in yeast cells.[138] In a 2009 study, the lifespans of mice fed rapamycin were increased between 28 and 38% from the beginning of treatment, or 9 to 14% in total increased maximum lifespan. Of particular note, the treatment began in mice aged 20 months, the equivalent of 60 human years.[139] Rapamycin has subsequently been shown to extend mouse lifespan in several separate experiments,[140][141] and is now being tested for this purpose in nonhuman primates (the marmoset monkey).[142]

Cancer geneticist Ronald A. DePinho and his colleagues published research in mice where telomerase activity was first genetically removed. Then, after the mice had prematurely aged, they restored telomerase activity by reactivating the telomerase gene. As a result, the mice were rejuvenated: Shrivelled testes grew back to normal and the animals regained their fertility. Other organs, such as the spleen, liver, intestines and brain, recuperated from their degenerated state. “[The finding] offers the possibility that normal human ageing could be slowed by reawakening the enzyme in cells where it has stopped working” says Ronald DePinho. However, activating telomerase in humans could potentially encourage the growth of tumours.[143]

Most known genetic interventions in C. elegans increase lifespan by 1.5 to 2.5-fold. As of 2009[update], the record for lifespan extension in C. elegans is a single-gene mutation which increases adult survival by tenfold.[49] The strong conservation of some of the mechanisms of ageing discovered in model organisms imply that they may be useful in the enhancement of human survival. However, the benefits may not be proportional; longevity gains are typically greater in C. elegans than fruit flies, and greater in fruit flies than in mammals. One explanation for this is that mammals, being much longer-lived, already have many traits which promote lifespan.[49]

Some research effort is directed to slow ageing and extend healthy lifespan.[144][145][146]

The US National Institute on Aging currently funds an intervention testing programme, whereby investigators nominate compounds (based on specific molecular ageing theories) to have evaluated with respect to their effects on lifespan and age-related biomarkers in outbred mice.[147] Previous age-related testing in mammals has proved largely irreproducible, because of small numbers of animals and lax mouse husbandry conditions.[citation needed] The intervention testing programme aims to address this by conducting parallel experiments at three internationally recognised mouse ageing-centres, the Barshop Institute at UTHSCSA, the University of Michigan at Ann Arbor and the Jackson Laboratory.

Several companies and organisations, such as Google Calico, Human Longevity, Craig Venter, Gero,[148]SENS Research Foundation, and Science for Life Extension in Russia,[149] declared stopping or delaying ageing as their goal.

Prizes for extending lifespan and slowing ageing in mammals exist. The Methuselah Foundation offers the Mprize. Recently, the $1 Million Palo Alto Longevity Prize was launched. It is a research incentive prize to encourage teams from all over the world to compete in an all-out effort to “hack the code” that regulates our health and lifespan. It was founded by Joon Yun.[150][151][152][153][154]

Different cultures express age in different ways. The age of an adult human is commonly measured in whole years since the day of birth. Arbitrary divisions set to mark periods of life may include: juvenile (via infancy, childhood, preadolescence, adolescence), early adulthood, middle adulthood, and late adulthood. More casual terms may include “teenagers,” “tweens,” “twentysomething”, “thirtysomething”, etc. as well as “vicenarian”, “tricenarian”, “quadragenarian”, etc.

Most legal systems define a specific age for when an individual is allowed or obliged to do particular activities. These age specifications include voting age, drinking age, age of consent, age of majority, age of criminal responsibility, marriageable age, age of candidacy, and mandatory retirement age. Admission to a movie for instance, may depend on age according to a motion picture rating system. A bus fare might be discounted for the young or old. Each nation, government and non-governmental organisation has different ways of classifying age. In other words, chronological ageing may be distinguished from “social ageing” (cultural age-expectations of how people should act as they grow older) and “biological ageing” (an organism’s physical state as it ages).[155]

In a UNFPA report about ageing in the 21st century, it highlighted the need to “Develop a new rights-based culture of ageing and a change of mindset and societal attitudes towards ageing and older persons, from welfare recipients to active, contributing members of society.”[156] UNFPA said that this “requires, among others, working towards the development of international human rights instruments and their translation into national laws and regulations and affirmative measures that challenge age discrimination and recognise older people as autonomous subjects.”[156] Older persons make contributions to society including caregiving and volunteering. For example, “A study of Bolivian migrants who [had] moved to Spain found that 69% left their children at home, usually with grandparents. In rural China, grandparents care for 38% of children aged under five whose parents have gone to work in cities.”[156]

Population ageing is the increase in the number and proportion of older people in society. Population ageing has three possible causes: migration, longer life expectancy (decreased death rate) and decreased birth rate. Ageing has a significant impact on society. Young people tend to have fewer legal privileges (if they are below the age of majority), they are more likely to push for political and social change, to develop and adopt new technologies, and to need education. Older people have different requirements from society and government, and frequently have differing values as well, such as for property and pension rights.[157]

In the 21st century, one of the most significant population trends is ageing.[158] Currently, over 11% of the world’s current population are people aged 60 and older and the United Nations Population Fund (UNFPA) estimates that by 2050 that number will rise to approximately 22%.[156] Ageing has occurred due to development which has enabled better nutrition, sanitation, health care, education and economic well-being. Consequently, fertility rates have continued to decline and life expectancy have risen. Life expectancy at birth is over 80 now in 33 countries. Ageing is a “global phenomenon,” that is occurring fastest in developing countries, including those with large youth populations, and poses social and economic challenges to the work which can be overcome with “the right set of policies to equip individuals, families and societies to address these challenges and to reap its benefits.”[159]

As life expectancy rises and birth rates decline in developed countries, the median age rises accordingly. According to the United Nations, this process is taking place in nearly every country in the world.[160] A rising median age can have significant social and economic implications, as the workforce gets progressively older and the number of old workers and retirees grows relative to the number of young workers. Older people generally incur more health-related costs than do younger people in the workplace and can also cost more in worker’s compensation and pension liabilities.[161] In most developed countries an older workforce is somewhat inevitable. In the United States for instance, the Bureau of Labor Statistics estimates that one in four American workers will be 55 or older by 2020.[161]

Among the most urgent concerns of older persons worldwide is income security. This poses challenges for governments with ageing populations to ensure investments in pension systems continues in order to provide economic independence and reduce poverty in old age. These challenges vary for developing and developed countries. UNFPA stated that, “Sustainability of these systems is of particular concern, particularly in developed countries, while social protection and old-age pension coverage remain a challenge for developing countries, where a large proportion of the labour force is found in the informal sector.”[156]

The global economic crisis has increased financial pressure to ensure economic security and access to health care in old age. In order to elevate this pressure “social protection floors must be implemented in order to guarantee income security and access to essential health and social services for all older persons and provide a safety net that contributes to the postponement of disability and prevention of impoverishment in old age.”[156]

It has been argued that population ageing has undermined economic development.[162] Evidence suggests that pensions, while making a difference to the well-being of older persons, also benefit entire families especially in times of crisis when there may be a shortage or loss of employment within households. A study by the Australian Government in 2003 estimated that “women between the ages of 65 and 74 years contribute A$16 billion per year in unpaid caregiving and voluntary work. Similarly, men in the same age group contributed A$10 billion per year.”[156]

Due to increasing share of the elderly in the population, health care expenditures will continue to grow relative to the economy in coming decades. This has been considered as a negative phenomenon and effective strategies like labour productivity enhancement should be considered to deal with negative consequences of ageing.[163]

In the field of sociology and mental health, ageing is seen in five different views: ageing as maturity, ageing as decline, ageing as a life-cycle event, ageing as generation, and ageing as survival.[164] Positive correlates with ageing often include economics, employment, marriage, children, education, and sense of control, as well as many others. The social science of ageing includes disengagement theory, activity theory, selectivity theory, and continuity theory. Retirement, a common transition faced by the elderly, may have both positive and negative consequences.[165] As cyborgs currently are on the rise some theorists argue there is a need to develop new definitions of ageing and for instance a bio-techno-social definition of ageing has been suggested.[166]

With age inevitable biological changes occur that increase the risk of illness and disability. UNFPA states that,[159]

“A life-cycle approach to health care one that starts early, continues through the reproductive years and lasts into old age is essential for the physical and emotional well-being of older persons, and, indeed, all people. Public policies and programmes should additionally address the needs of older impoverished people who cannot afford health care.”

Many societies in Western Europe and Japan have ageing populations. While the effects on society are complex, there is a concern about the impact on health care demand. The large number of suggestions in the literature for specific interventions to cope with the expected increase in demand for long-term care in ageing societies can be organised under four headings: improve system performance; redesign service delivery; support informal caregivers; and shift demographic parameters.[167]

However, the annual growth in national health spending is not mainly due to increasing demand from ageing populations, but rather has been driven by rising incomes, costly new medical technology, a shortage of health care workers and informational asymmetries between providers and patients.[168] A number of health problems become more prevalent as people get older. These include mental health problems as well as physical health problems, especially dementia.

It has been estimated that population ageing only explains 0.2 percentage points of the annual growth rate in medical spending of 4.3% since 1970. In addition, certain reforms to the Medicare system in the United States decreased elderly spending on home health care by 12.5% per year between 1996 and 2000.[169]

Positive self-perception of health has been correlated with higher well-being and reduced mortality in the elderly.[170][171] Various reasons have been proposed for this association; people who are objectively healthy may naturally rate their health better than that of their ill counterparts, though this link has been observed even in studies which have controlled for socioeconomic status, psychological functioning and health status.[172] This finding is generally stronger for men than women,[171] though this relationship is not universal across all studies and may only be true in some circumstances.[172]

As people age, subjective health remains relatively stable, even though objective health worsens.[173] In fact, perceived health improves with age when objective health is controlled in the equation.[174] This phenomenon is known as the “paradox of ageing.” This may be a result of social comparison;[175] for instance, the older people get, the more they may consider themselves in better health than their same-aged peers.[176] Elderly people often associate their functional and physical decline with the normal ageing process.[177][178]

The concept of successful ageing can be traced back to the 1950s and was popularised in the 1980s. Traditional definitions of successful ageing have emphasised absence of physical and cognitive disabilities.[179] In their 1987 article, Rowe and Kahn characterised successful ageing as involving three components: a) freedom from disease and disability, b) high cognitive and physical functioning, and c) social and productive engagement.[180]

The ancient Greek dramatist Euripides (5th century BC) describes the multiply-headed mythological monster Hydra as having a regenerative capacity which makes it immortal, which is the historical background to the name of the biological genus Hydra. The Book of Job (c. 6th century BC) describes human lifespan as inherently limited and makes a comparison with the innate immortality that a felled tree may have when undergoing vegetative regeneration.[181]

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Ageing – Wikipedia

Clomiphene Citrate (Clomid) in Men – A Testosterone …

08-12-2016 9:41 am

A Testosterone Therapy Alternative for Men with Low Testosterone Levels

Whether you are a 30, 50, 80 or even 110 year old man, having low testosterone levels (hypogonadism) is neither fun nor healthy. The symptoms of low testosterone in men range from lack of energy, depressed mood, loss of vitality, muscle atrophy (sarcopenia), muscles aches, low libido, erectile dysfunction, and weight gain…to bone loss (osteopenia), osteoporosis, mild anemia, increased risk of Alzheimer’s, increased risk of high-grade prostate cancer, and increased risk of death due to all causes.1

As you may know, low testosterone in men may be caused by problems in the testes (or gonads). This is called primary hypogonadism and can be brought on by the mumps, testicular trauma, or testicular cancer, etc., and can only be treated with testosterone replacement therapy. However, the more common causes of low testosterone/hypogonadism result from problems in the pituitary gland and/or hypothalamus in a man’s brain. Low testosterone levels caused by such “brain problems” are collectively described as secondary hypogonadism or hypogonadotropic hypogonadism and may result from depression/anxiety, head trauma, iron overload, anabolic steroid overdosing, diabetes, sleep deprivation, or some medications.

Traditionally, if low testosterone is diagnosed, testosterone replacement therapy is prescribed, and it most commonly comes in the form of a cream, gel, pellet, patch, and by injection. And although these types of therapy are effective, some methods are better than others, and there are side-effects with all of them. For example, testicular shrinkage, gynecomastia (breast enlargement), low sperm count/sterility, and polycythemia (overproduction of red blood cells) are common side-effects of testosterone replacement therapy (for many sufferers, these side-effects are mostly treatable or considered “worth it” by the patient).

However, specifically due to the sterility side-effect, such testosterone treatments aren’t a good option for men who want to have children. In these (usually young) hypogonadal men, clomiphene citrate (CC pill, or Clomid) and/or human chorionic gonadotropin (HCG) have been used (by specialists) for decades to increase testosterone production, increase sperm production, and increase fertility. Both these therapies effectively help signal the testes to produce testosterone and thereby increase testosterone levels (assuming of course the cause of the initial problem is not in the testes’ ability to make testosterone). See “David” below for an oversimplified diagram of how clomiphene, HCG, and testosterone work within the hypothalamic-pituitary-testicular axis.

In a healthy male, the pituitary gland in the brain releases luteinizing hormone (LH) into the blood stream, which signals the testes to GO and produce testosterone. After testosterone has been produced it naturally converts to some estrogen (yes, theres estrogen in men too) and this estrogen acts as a STOP signal to the pituitary to stop making LH. It is a delicate system of checks and balances which I have simplified here for our purposes.

Clomid (clomiphene citrate, or CC pill)works by blocking estrogen at the pituitary and hypothalamus. Thus, the usual estrogen message to “STOP” production of LH is essentially silenced, and therefore the pituitary makes more LH and there is an increased “GO” signal to produce testosterone in the testes. HCG works by mimicking LH, which also increases the “GO” signal to produce more testosterone in the testes. Prescribing testosterone for a man, however, does the opposite of what clomiphene and HCG do.

With traditional testosterone replacement therapy, the brain (hypothalamus and pituitary) gets the message that there is plenty of testosterone being made in the testes, so much so that it doesn’t need to make anymore. Subsequently, the pituitary stops producing LH, and the natural production of testosterone (and sperm) in the testes ceases, which is why traditional testosterone replacement results in testicular shrinkage and low sperm count…a man’s testosterone and sperm manufacturing plant is essentially shut off.

Clomiphene citrate (CC pill) and/or HCG do not turn off the testosterone manufacturing plant but rather turn it back on or reboot it. While some hypogonadal men require continuous use of clomiphene, for others it can be used for a 3-6 month time period and then discontinued. And, the checks and balances system is not interrupted, so there aren’t the testosterone replacement side-effects which occur due to intentional or unintentional testosterone overdosing. Most interestingly, although it used to be thought that clomiphene and/or HCG only worked on young men, in the past decade or so it has been used effectively in older men too.

The 5 Main Reasons Clomiphene Citrate (CC pill, or Clomid) May be a Good Alternative to Testosterone Replacement Therapy in Men with Low Testosterone Due to Secondary Hypogonadism:

1. Clomiphene citrate (CC pill) stimulates the body’s own production of testosterone

2. Clomiphene citrate (CC pill) doesn’t interfere with the body’s checks and balances of testosterone

3. Clomiphene citrate (CC pill)comes as a pill easily administered by mouth

4. Clomiphene citrate (CC pill) is generic and very cheap2

5. Clomiphene citrate (CC pill) has little side-effects and low risk of developing these side-effects3

The 5 Main Reasons Clomiphene Citrate (CC pill, or Clomid) is Not Usually Prescribed to Men with Low Testosterone Due to Secondary Hypogonadism:

1. Most doctors aren’t aware of the efficacy and safety of clomiphene use in men

2. Most doctors think of Clomid as a “women’s drug” to increase fertility

3. Clomid is FDA approved only for use in women

4. Clomid use in men is considered “off label”

5. Clomiphene citrate (CC pill) is now generic and really inexpensive so it’s not advertised very much

Note: HCG is more commonly known and prescribed for secondary hypogonadism in men but it involves injection and is expensive, so if clomiphene works alone I think that is preferred.

The 4 Main Risks of Using Clomiphene Citrate (CC pill, or Clomid) in Men with Low Testosterone Due to Secondary Hypogonadism:

1. Very rarely, visual changes may occur which are reversible with discontinuation

2. In older men, there is a reported increased risk of pyospermia (a noninfectious increase in white blood cells in semen, with unseen detriment)

3. Clomiphene citrate (CC pill)is a drug which is not bioidentical. This means it’s molecular structure doesn’t mimic a compound naturally found in the human body. And, correspondingly, clomiphene citrate (CC pill) doesn’t have a known natural function in the human body and thus may at some point manifest a currently unknown side-effect in men. This latter, however, is a theoretical risk because for more than 40 years clomiphene use in men has only shown the risks above.

4. Clomiphene may not work…especially in older men who in addition to secondary hypogonadism may also have primary hypogonadism; or in men with an unresolved chronic disease4

In conclusion, in the appropriate male patient, clomiphene citrate (CC pill, or Clomid) may be a good alternative to both short and long-term testosterone replacement therapy. Regardless, just like testosterone replacement, clomiphene citrate (CC pill) must be administered and monitored by a competent physician. If you are interested in becoming a patient, click here for more info.

I look forward to meeting you in consultation.

Dr. Shira Miller p.s. Thank you for all your questions and comments. I apologize but I cannot give personal medical advice. The most commonquestions in this blog will be answered in my upcoming book. SM

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Clomiphene Citrate (Clomid) in Men – A Testosterone …

Stimulant – Wikipedia

08-12-2016 9:41 am

Stimulants (also referred to as psychostimulants) are psychoactive drugs that induce temporary improvements in either mental or physical functions or both. Examples of these kinds of effects may include enhanced alertness, wakefulness, and locomotion, among others. Due to their rendering a characteristic “up” feeling, stimulants are also occasionally referred to as “uppers”. Depressants or “downers”, which decrease mental and/or physical function, are in stark contrast to stimulants and are considered to be the functionally opposite drug class. Stimulants are widely used throughout the world as prescription medicines as well as without a prescription (either legally or illicitly) as performance-enhancing or recreational drugs. Some examples of legal non-presciption stimulants are caffeine and pseudophedrine. Some examples of prescription stimulants are Adderall (amphetamine salts), Ritalin (methylphenidate), amphetamines, and methamphetamine. Examples of Illicit stimulants (illegal stimulants) are cocaine, crystal meth.[1]

Stimulants produce a variety of different kinds of effects by enhancing the activity of the central and peripheral nervous systems. Common effects, which vary depending on the substance and dosage in question, may include enhanced alertness, awareness, wakefulness, endurance, productivity, and motivation, increased arousal, locomotion, heart rate, and blood pressure, and the perception of a diminished requirement for food and sleep. Many stimulants are also capable of improving mood and relieving anxiety, and some can even induce feelings of euphoria. However different effects are often dose related, such as amphetamine causing anxiety, dysthymia, hyperactivity and potentially heart failure at high doses, but relieving anxiety, producing euthymia or euphoria, reducing hyperactivity and being generally free of serious side effects at moderate doses used in clinical medicine. Stimulants exert their effects through a number of different pharmacological mechanisms, the most prominent of which include facilitation of norepinephrine (noradrenaline) and/or dopamine activity (e.g., via monoamine transporter inhibition or reversal),[2]adenosine receptor antagonism, and nicotinic acetylcholine receptor agonism.

Stimulants are used both individually and clinically for therapeutic purposes in the treatment of a number of indications, including the following:

Stimulants are the most effective, most commonly prescribed medications for ADHD.[8] The most common stimulant medications are substituted phenethylamines: amphetamine, methylphenidate (Ritalin, Metadate, Concerta), dexmethylphenidate (Focalin), dextroamphetamine (Dexedrine, Zenzedi), mixed amphetamine salts (Adderall),[9]dextromethamphetamine (Desoxyn)[10] and lisdexamfetamine (Vyvanse).[11] Controlled-release formulations may allow once or twice daily administration of medication. Once daily morning administration is especially helpful for children preferring not to take their medication in the middle of the school day. Several controlled-release methods are used.

Ampakines are a class of compounds observed to enhance attention span and alertness, and facilitate learning and memory in clinical trials. They take their name from the glutamatergic AMPA receptor with which they strongly interact.

These stimulants tend to increase alertness without the peripheral (body) effects or addiction/tolerance/abuse potential of “traditional” stimulants (such as amphetamine),[medical citation needed] as they lack direct dopaminergic action. Their effect on sleep structure is not fully established and may reduce quality of sleep. The ampakine CX717, when administered at doses necessary to reduce the effects of sleep deprivation, reduced subsequent stage 4 and slow-wave recovery sleep.[12] Ampakines such as ampalex and CX717 have been developed but are awaiting further research before being commercially released. They have been investigated by DARPA for potential use in increasing military effectiveness.[13]

A wakefulness-promoting agent (eugeroic) is a type of psychoactive drug that improves wakefulness and alertness, and reduces tiredness, drowsiness, and the need for sleep. They are used mainly in the treatment of sleeping disorders, excessive daytime sleepiness, and narcolepsy, though they are also used merely to counteract fatigue and lethargy and to enhance motivation and productivity. Wakefulness-promoting agents appear to function primarily by increasing catecholaminergic (adrenergic, dopaminergic) and histaminergic activity in the brain. Unlike many other stimulants, eugeroics are relatively non-addictive and non-dependence-forming.[medical citation needed]

The prototype drug in this class is modafinil, and other drugs include adrafinil, hydrafinil, and armodafinil. The primary difference between these drugs and amphetamine-like stimulants is that wakefulness-promoting agents trigger activation of neurons in the hypothalamus-based wakefulness circuits, as opposed to producing diffuse neuronal activation.[14]

The functional opposites of wakefulness-promoting agents would be hypnotics/sedatives like antihistamines, opioids, and benzodiazepines.

Classifying stimulants is difficult, because of the large number of classes the drugs occupy, and the fact that they may belong to multiple classes; for example, ecstasy is a substituted methylenedioxyphenethylamine as well as a substituted amphetamine (and consequently, a substituted phenethylamine as well).

When referring to stimulants, the parent drug (e.g., amphetamine) will always be expressed in the singular; with the word “substituted” placed before the parent drug (substituted amphetamines).

Major stimulant classes include phenethylamines and their daughter class substituted amphetamines.

Substituted amphetamines are a group of phenylethylamine stimulants such as amphetamine and methamphetamine. With the exception of cathinones, many drugs in this class work primarily by activating trace amine-associated receptor 1 (TAAR1);[15] in turn, this causes reuptake inhibition and effluxion, or release, of dopamine, norepinephrine, and serotonin.[15] An additional mechanism of some substituted amphetamines is the release of neurotransmitters from synaptic vesicles into the cytosol, or intracellular fluid of the presynaptic neuron.[16]

Amphetamines-type stimulants are often used for their therapeutic effects. Physicians sometimes prescribe amphetamine to treat major depression, where subjects do not respond well to traditional SSRI medications,[citation needed] but evidence supporting this use is poor/mixed.[17] Notably, two recent large phase III studies of lisdexamfetamine (a prodrug to amphetamine) as an adjunct to an SSRI or SNRI in the treatment of major depressive disorder showed no further benefit relative to placebo in effectiveness.[18] Numerous studies have demonstrated the effectiveness of drugs such as Adderall (a mixture of salts of amphetamine and dextroamphetamine) in controlling symptoms associated with ADD/ADHD. Due to their availability and fast-acting effects, substituted amphetamines are prime candidates for abuse.[19]

primary pathway

minor pathway

Dopamine is one of the principal neurotransmitters involved with stimulant activity in the brain, (others being norepinephrine and serotonin). Increase in its precursors may result in increased dopamine biosynthesis, especially in malnourished individuals. However levels of the enzyme tyrosine hydroxylase ultimately limit the biosynthesis regardless of increased tyrosine.

L-Tyrosine is the precursor that is ‘closest’ to being dopamine among those supplements legally available without prescription in most jurisdictions. It is converted by tyrosine hydroxylase into L-Dopa. Some of this L-Dopa is converted into dopamine and norepinephrine. Because tyrosine competes with other amino acids for entry into the brain supplement makers recommend tyrosine be taken on an empty stomach. However tyrosine hydroxylase is the rate limiting factor and even large dosages recommended by most supplement companies may not produce any noticeable effect. L-Phenylalanine is ‘one step back’ from L-Tyrosineit must be converted into tyrosine before the tyrosine can be converted into L-Dopa, which in turn becomes dopamine. Dopamine is also the direct precursor of norepinephrine.

Amphetamine is a potent central nervous system (CNS) stimulant of the phenethylamine class that is used in the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy.[23] Amphetamine was discovered in 1887 and exists as two enantiomers: levoamphetamine and dextroamphetamine.[note 1][24]Amphetamine refers to equal parts of the enantiomers, i.e., 50%levoamphetamine and 50%dextroamphetamine.[25][26] Historically, it has been used to treat nasal congestion, depression, and obesity.[24][27] Amphetamine is also used as a performance and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant.[28][29][30][31] Although it is a prescription medication in many countries, unauthorized possession and distribution of amphetamine is often tightly controlled due to the significant health risks associated with uncontrolled or heavy use.[32][33] As a consequence, amphetamine is illegally synthesized by clandestine chemists, trafficked, and sold.[34] Based upon drug and drug precursor seizures worldwide, illicit amphetamine production and trafficking is much less prevalent than that of methamphetamine.[34]

The first pharmaceutical amphetamine was Benzedrine, a brand of inhalers used to treat a variety of conditions.[24][27] Because the dextro isomer has greater stimulant properties, Benzedrine was gradually discontinued in favor of formulations containing all or mostly dextroamphetamine. Presently, it is typically prescribed as Adderall, dextroamphetamine (e.g., Dexedrine), or the inactive prodrug lisdexamfetamine (e.g., Vyvanse).[24][35] Amphetamine, through activation of a trace amine receptor, increases biogenic amine and excitatory neurotransmitter activity in the brain, with its most pronounced effects targeting the catecholamine neurotransmitters norepinephrine and dopamine.[15] At therapeutic doses, this causes emotional and cognitive effects such as euphoria, change in libido, increased arousal, and improved cognitive control.[29][30][36] Likewise, it induces physical effects such as decreased reaction time, fatigue resistance, and increased muscle strength.[28]

In contrast, much larger doses of amphetamine are likely to impair cognitive function and induce rapid muscle breakdown.[23][29][37]Substance dependence (i.e., addiction) is a serious risk of amphetamine abuse, but only rarely arises from proper medical use.[23][38] Very high doses can result in a psychosis (e.g., delusions and paranoia), which very rarely occurs at therapeutic doses even during long-term use.[39][40] As recreational doses are generally much larger than prescribed therapeutic doses, recreational use carries a far greater risk of serious side effects.[23][37]

Amphetamine is the parent compound of its own structural class, the (substituted) amphetamines, which includes prominent substances such as bupropion, cathinone, ecstasy, and methamphetamine.[41][42] It is chemically related to methamphetamine; however, unlike methamphetamine, its salts lack sufficient volatility to be smoked.[41] During long-term treatment in humans, amphetamine has been shown to normalize, or improve, brain function, in particular in the right caudate nucleus;[43][44] in contrast, methamphetamine induces permanent reductions in brain structure and function.[45][46] Amphetamine is also chemically related to the naturally occurring trace amines, to be specific phenethylamine and N-methylphenethylamine, both of which produced within the human body.[42]

Caffeine is a stimulant compound belonging to the xanthine class of chemicals naturally found in coffee, tea, and (to a lesser degree) cocoa or chocolate. It is included in many soft drinks, as well as a larger amount in energy drinks. Caffeine is the world’s most widely used psychoactive drug and by far the most common stimulant. In North America, 90% of adults consume caffeine daily.[47] A few jurisdictions restrict its sale and use. Caffeine is also included in some medications, usually for the purpose of enhancing the effect of the primary ingredient, or reducing one of its side-effects (especially drowsiness). Tablets containing standardized doses of caffeine are also widely available.

Ephedrine is a sympathomimetic amine similar in molecular structure to the well-known drugs phenylpropanolamine and methamphetamine, as well as to the important neurotransmitter epinephrine (adrenaline). Ephedrine is commonly used as a stimulant, appetite suppressant, concentration aid, and decongestant, and to treat hypotension associated with anaesthesia.

In chemical terms, it is an alkaloid with a phenethylamine skeleton found in various plants in the genus Ephedra (family Ephedraceae). It works mainly by increasing the activity of norepinephrine (noradrenaline) on adrenergic receptors.[48] It is most usually marketed as the hydrochloride or sulfate salt.

The herb m hung (Ephedra sinica), used in traditional Chinese medicine (TCM), contains ephedrine and pseudoephedrine as its principal active constituents. The same may be true of other herbal products containing extracts from other Ephedra species.

3,4-Methylenedioxymethamphetamine (MDMA, ecstasy, or molly), typically comes as tablets, capsules, and in powder/crystal form. Briefly used by some psychotherapists as an adjunct to therapy, the drug became popular recreationally and the DEA listed MDMA as a Schedule I controlled substance, prohibiting most medical studies and applications. MDMA is known for its entactogenic properties. The stimulant effects of MDMA include hypertension, anorexia (appetite loss), euphoria, social disinhibition, insomnia (enhanced wakefulness/inability to sleep), improved energy, increased arousal, and increased perspiration, among others.

MDMA differs from most stimulants in that its primary pharmacological effect is on the neurotransmitter serotonin rather than dopamine, epinephrine, or norepinephrine. Because of this, it is considered to be primarily an entactogen or an empathogen.

Methylenedioxypyrovalerone (MDPV) is a psychoactive drug with stimulant properties that acts as a norepinephrine-dopamine reuptake inhibitor (NDRI).[49] It was first developed in the 1960s by a team at Boehringer Ingelheim.[50] MDPV remained an obscure stimulant until around 2004, when it was reported to be sold as a designer drug. Products labeled as bath salts containing MDPV were previously sold as recreational drugs in gas stations and convenience stores in the United States, similar to the marketing for Spice and K2 as incense.[51][52]

Incidents of psychological and physical harm have been attributed to MDPV use.[53][54]

Mephedrone is a synthetic stimulant drug of the amphetamine and cathinone classes. Slang names include drone[55] and MCAT.[56] It is reported to be manufactured in China and is chemically similar to the cathinone compounds found in the khat plant of eastern Africa. It comes in the form of tablets or a powder, which users can swallow, snort, or inject, producing similar effects to MDMA, amphetamines, and cocaine.

Mephedrone was first synthesized in 1929, but did not become widely known until it was rediscovered in 2003. By 2007, mephedrone was reported to be available for sale on the Internet; by 2008 law enforcement agencies had become aware of the compound; and, by 2010, it had been reported in most of Europe, becoming particularly prevalent in the United Kingdom. Mephedrone was first made illegal in Israel in 2008, followed by Sweden later that year. In 2010, it was made illegal in many European countries, and, in December 2010, the EU ruled it illegal. In Australia, New Zealand, and the USA, it is considered an analog of other illegal drugs and can be controlled by laws similar to the Federal Analog Act. In September 2011, the USA temporarily classified mephedrone as illegal, in effect from October 2011.

Methamphetamine (contracted from N-methyl-alpha-methylphenethylamine) is a neurotoxin and potent psychostimulant of the phenethylamine and amphetamine classes that is used to treat attention deficit hyperactivity disorder (ADHD) and obesity.[45][57][46] Methamphetamine exists as two enantiomers, dextrorotary and levorotary.[58][59] Dextromethamphetamine is a stronger CNS stimulant than levomethamphetamine;[37][58][59] however, both are addictive and produce the same toxicity symptoms at high doses.[59] Although rarely prescribed due to the potential risks, methamphetamine hydrochloride is approved by the United States Food and Drug Administration (USFDA) under the trade name Desoxyn.[57] Recreationally, methamphetamine is used to increase sexual desire, lift the mood, and increase energy, allowing some users to engage in sexual activity continuously for several days straight.[57][60]

Methamphetamine may be sold illicitly, either as pure dextromethamphetamine or in an equal parts mixture of the right- and left-handed molecules (i.e., 50%levomethamphetamine and 50%dextromethamphetamine).[60] Both dextromethamphetamine and racemic methamphetamine are schedule II controlled substances in the United States.[57] Also, the production, distribution, sale, and possession of methamphetamine is restricted or illegal in many other countries due to its placement in schedule II of the United Nations Convention on Psychotropic Substances treaty.[61][62] In contrast, levomethamphetamine is an over-the-counter drug in the United States.[note 2]

In low doses, methamphetamine can cause an elevated mood and increase alertness, concentration, and energy in fatigued individuals.[37][57] At higher doses, it can induce psychosis, rhabdomyolysis, and cerebral hemorrhage.[37][57] Methamphetamine is known to have a high potential for abuse and addiction.[37][57] Recreational use of methamphetamine may result in psychosis or lead to post-withdrawal syndrome, a withdrawal syndrome that can persist for months beyond the typical withdrawal period.[65] Unlike amphetamine and cocaine, methamphetamine is neurotoxic to humans, damaging both dopamine and serotonin neurons in the central nervous system (CNS).[45][46] Entirely opposite to the long-term use of amphetamine, there is evidence that methamphetamine causes brain damage from long-term use in humans;[45][46] this damage includes adverse changes in brain structure and function, such as reductions in gray matter volume in several brain regions and adverse changes in markers of metabolic integrity.[43][44][46]

Nicotine is the active chemical constituent in tobacco, which is available in many forms, including cigarettes, cigars, chewing tobacco, and smoking cessation aids such as nicotine patches, nicotine gum, and electronic cigarettes. Nicotine is used widely throughout the world for its stimulating and relaxing effects.

Phenylpropanolamine (PPA; Accutrim; -hydroxyamphetamine), also known as the stereoisomers norephedrine and norpseudoephedrine, is a psychoactive drug of the phenethylamine and amphetamine chemical classes that is used as a stimulant, decongestant, and anorectic agent.[66] It is commonly used in prescription and over-the-counter cough and cold preparations. In veterinary medicine, it is used to control urinary incontinence in dogs under trade names Propalin and Proin.

In the United States, PPA is no longer sold without a prescription due to a proposed increased risk of stroke in younger women. In a few countries in Europe, however, it is still available either by prescription or sometimes over-the-counter. In Canada, it was withdrawn from the market on 31 May 2001.[67] In India, human use of PPA and its formulations were banned on 10 February 2011.[68]

Propylhexedrine (Hexahydromethamphetamine, Obesin) is a stimulant medication, sold over-the-counter in the United States as the cold medication Benzedrex.[69] The drug has also been used as an appetite suppressant in Europe. Propylhexedrine is not an amphetamine, though it is structurally similar; it is instead a cycloalkylamine, and thus has stimulant effects that are less potent than similarly structured amphetamines, such as methamphetamine.

The abuse potential of propylhexedrine is fairly limited, due its limited routes of administration: in the United States, Benzedrex is only available as an inhalant, mixed with lavender oil and menthol. These ingredients cause unpleasant tastes, and abusers of the drug have reported unpleasant “menthol burps.” Injection of the drug has been found to cause transient diplopia and brain stem dysfunction.[70][71][72]

Dimethylamylamine is a stimulant drug, once sold in over-the-counter workout supplements and study aids in the United States as in the supplement Jack 3D, but it was later discontinued. Dimethylamylamine is not an amphetamine, though it is structurally similar, and thus has stimulant effects that are less potent than similarly structured amphetamines, such as amphetamine.

Pseudoephedrine is a sympathomimetic drug of the phenethylamine and amphetamine chemical classes. It may be used as a nasal/sinus decongestant, as a stimulant,[73] or as a wakefulness-promoting agent.[74]

The salts pseudoephedrine hydrochloride and pseudoephedrine sulfate are found in many over-the-counter preparations, either as a single ingredient or (more commonly) in combination with antihistamines, guaifenesin, dextromethorphan, and/or paracetamol (acetaminophen) or another NSAID (such as aspirin or ibuprofen).

Khat is a flowering plant native to the Horn of Africa and the Arabian Peninsula.[75][76]

Khat contains a monoamine alkaloid called cathinone, a “keto-amphetamine”, that is said to cause excitement, loss of appetite, and euphoria. In 1980, the World Health Organization (WHO) classified it as a drug of abuse that can produce mild to moderate psychological dependence (less than tobacco or alcohol),[77] although the WHO does not consider khat to be seriously addictive.[76] It is a controlled substance in some countries, such as the United States, Canada, and Germany, while its production, sale, and consumption are legal in other nations, including Djibouti, Ethiopia, Somalia, and Yemen.[78]

Cocaine is an SNDRI. Cocaine is made from the leaves of the coca shrub, which grows in the mountain regions of South American countries such as Bolivia, Colombia, and Peru. In Europe, North America, and some parts of Asia, the most common form of cocaine is a white crystalline powder. Cocaine is a stimulant but is not normally prescribed therapeutically for its stimulant properties, although it sees clinical use as a local anesthetic, in particular in ophthalmology. Most cocaine use is recreational and its abuse potential is high (albeit higher than amphetamine), and so its sale and possession are strictly controlled in most jurisdictions. Other tropane derivative drugs related to cocaine are also known such as troparil and lometopane but have not been widely sold or used recreationally.[79]

Abuse of central nervous system (CNS) stimulants is common. Addiction to some CNS stimulants can quickly lead to medical, psychiatric, and psychosocial deterioration. Drug tolerance, dependence, and sensitization as well as a withdrawal syndrome can occur.[80]

Stimulants enhance the activity of the central and peripheral nervous systems. Common effects may include increased alertness, awareness, wakefulness, endurance, productivity, and motivation, arousal, locomotion, heart rate, and blood pressure, and a diminished desire for food and sleep.

Use of stimulants may cause the body to reduce significantly its production of natural body chemicals that fulfill similar functions. Until the body reestablishes its normal state, once the effect of the ingested stimulant has worn off the user may feel depressed, lethargic, confused, and miserable. This is referred to as a “crash”, and may provoke reuse of the stimulant.

The presence of stimulants in the body may be tested by a variety of procedures. Serum and urine are the common sources of testing material although saliva is sometimes used. Commonly used tests include chromatography, immunologic assay, and mass spectrometry.[81] Patients taking ADHD-prescribed, Adderall-type amphetamine compounds are commonly surprised upon being tested as “positive” for “meth”, or methamphetamine (Desoxynits licit, FDA-licensed, medicinal form) in forensically unsophisticated urinalysis, as methamphetamine is the active ingredient of the drug Desoxyn, and is chemically similar to the active ingredients of other ADHD medications.

Although useful in the treatment of ADHD, stimulants are controlled II substances with a history of preclinical and human studies showing potential abuse liability.

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Low-carbohydrate diet – Wikipedia

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Low-carbohydrate diets or low-carb diets are dietary programs that restrict carbohydrate consumption, often for the treatment of obesity or diabetes. Foods high in easily digestible carbohydrates (e.g., sugar, bread, pasta) are limited or replaced with foods containing a higher percentage of fats and moderate protein (e.g., meat, poultry, fish, shellfish, eggs, cheese, nuts, and seeds) and other foods low in carbohydrates (e.g., most salad vegetables such as spinach, kale, chard and collards), although other vegetables and fruits (especially berries) are often allowed. The amount of carbohydrate allowed varies with different low-carbohydrate diets.

Such diets are sometimes ‘ketogenic’ (i.e., they restrict carbohydrate intake sufficiently to cause ketosis). The induction phase of the Atkins diet[1][2][3] is ketogenic.

The term “low-carbohydrate diet” is generally applied to diets that restrict carbohydrates to less than 20% of caloric intake, but can also refer to diets that simply restrict or limit carbohydrates to less than recommended proportions (generally less than 45% of total energy coming from carbohydrates).[4][5]

Low-carbohydrate diets are used to treat or prevent some chronic diseases and conditions, including cardiovascular disease, metabolic syndrome, auto-brewery syndrome, high blood pressure, and diabetes.[6][7]

Gary Taubes has argued that low-carbohydrate diets are closer to the ancestral diet of humans before the origin of agriculture, and humans are genetically adapted to diets low in carbohydrate.[8] Direct archaeological or fossil evidence on nutrition during the Paleolithic, when all humans subsisted by hunting and gathering, is limited, but suggests humans evolved from the vegetarian diets common to other great apes to one with a greater level of meat-eating.[9] Some close relatives of modern Homo sapiens, such as the Neanderthals, appear to have been almost exclusively carnivorous.[10]

A more detailed picture of early human diets before the origin of agriculture may be obtained by analogy to contemporary hunter-gatherers. According to one survey of these societies, a relatively low carbohydrate (2240% of total energy), animal food-centered diet is preferred “whenever and wherever it [is] ecologically possible”, and where plant foods do predominate, carbohydrate consumption remains low because wild plants are much lower in carbohydrate and higher in fiber than modern domesticated crops.[11] Primatologist Katherine Milton, however, has argued that the survey data on which this conclusion is based inflate the animal content of typical hunter-gatherer diets; much of it was based on early ethnography, which may have overlooked the role of women in gathering plant foods.[12] She has also highlighted the diversity of both ancestral and contemporary foraging diets, arguing no evidence indicates humans are especially adapted to a single paleolithic diet over and above the vegetarian diets characteristic of the last 30 million years of primate evolution.[13]

The origin of agriculture brought about a rise in carbohydrate levels in human diets.[14] The industrial age has seen a particularly steep rise in refined carbohydrate levels in Western societies, as well as urban societies in Asian countries, such as India, China, and Japan.

In 1797, John Rollo reported on the results of treating two diabetic Army officers with a low-carbohydrate diet and medications. A very low-carbohydrate, ketogenic diet was the standard treatment for diabetes throughout the 19th century.[15][16]

In 1863, William Banting, a formerly obese English undertaker and coffin maker, published “Letter on Corpulence Addressed to the Public”, in which he described a diet for weight control giving up bread, butter, milk, sugar, beer, and potatoes.[17] His booklet was widely read, so much so that some people used the term “Banting” for the activity usually called “dieting”.[18]

In 1888, James Salisbury introduced the Salisbury steak as part of his high-meat diet, which limited vegetables, fruit, starches, and fats to one-third of the diet.[original research?]

In the early 1900s Frederick Madison Allen developed a highly restrictive short term regime which was described by Walter R. Steiner at the 1916 annual convention of the Connecticut State Medical Society as The Starvation Treatment of Diabetes Mellitus.[19]:176177[20][21][22] People showing very high urine glucose levels were confined to bed and restricted to an unlimited supply of water, coffee, tea, and clear meat broth until their urine was “sugar free”; this took two to four days but sometimes up to eight.[19]:177 After the person’s urine was sugar-free food was re-introduced; first only vegetables with less than 5g of carbohydate per day, eventually adding fruits and grains to build up to 3g of carbohydrate per kilogram of body weight. Then eggs and meat were added, building up to 1g of protein/kg of body weight per day, then fat was added to the point where the person stopped losing weight or a maximum of 40 calories of fat per kilogram per day was reached. The process was halted if sugar appeared in the person’s urine.[19]:177178 This diet was often administered in a hospital in order to better ensure compliance and safety.[19]:179

In 1958, Richard Mackarness M.D. published Eat Fat and Grow Slim, a low-carbohydrate diet with much of the same advice and based on the same theories as those promulgated by Robert Atkins more than a decade later. Mackarness also challenged the “calorie theory” and referenced primitive diets such as the Inuit as examples of healthy diets with a low-carbohydrate and high-fat composition.

In 1967, Irwin Stillman published The Doctor’s Quick Weight Loss Diet. The “Stillman diet” is a high-protein, low-carbohydrate, and low-fat diet. It is regarded as one of the first low-carbohydrate diets to become popular in the United States.[23] Other low-carbohydrate diets in the 1960s included the Air Force diet[24] and the drinking man’s diet.[25]Austrian physician Wolfgang Lutz published his book Leben Ohne Brot (Life Without Bread) in 1967.[26] However, it was not well known in the English-speaking world.

In 1972, Robert Atkins published Dr. Atkins Diet Revolution, which advocated the low-carbohydrate diet he had successfully used in treating patients in the 1960s (having developed the diet from a 1963 article published in JAMA).[27] The book met with some success, but, because of research at that time suggesting risk factors associated with excess fat and protein, it was widely criticized by the mainstream medical community as being dangerous and misleading, thereby limiting its appeal at the time.[28] Among other things, critics pointed out that Atkins had done little real research into his theories and based them mostly on his clinical work. Later that decade, Walter Voegtlin and Herman Tarnower published books advocating the Paleolithic diet and Scarsdale diet, respectively, each meeting with moderate success.[29][not in citation given]

The concept of the glycemic index was developed in 1981 by David Jenkins to account for variances in speed of digestion of different types of carbohydrates. This concept classifies foods according to the rapidity of their effect on blood sugar levels with fast-digesting simple carbohydrates causing a sharper increase and slower-digesting complex carbohydrates, such as whole grains, a slower one.[30] The concept has been extended to include the amount of carbohydrate actually absorbed, as well, as a tablespoonful of cooked carrots is less significant overall than a large baked potato (effectively pure starch, which is efficiently absorbed as glucose), despite differences in glycemic indices.

In the 1990s, Atkins published an update from his 1972 book, Dr. Atkins New Diet Revolution, and other doctors began to publish books based on the same principles. This has been said to be the beginning of what the mass media call the “low carb craze” in the United States.[31] During the late 1990s and early 2000s, low-carbohydrate diets became some of the most popular diets in the US. By some accounts, up to 18% of the population was using one type of low-carbohydrate diet or another at the peak of their popularity,[32] and this use spread to many countries.[citation needed]Food manufacturers and restaurant chains like Krispy Kreme noted the trend, as it affected their businesses.[33] Parts of the mainstream medical community has denounced low-carbohydrate diets as being dangerous to health, such as the AHA in 2001,[34] the American Kidney Fund in 2002,[35] Low-carbohydrate advocates did some adjustments of their own, increasingly advocating controlling fat and eliminating trans fat.[36][37]

Proponents who appeared with new diet guides at that time like the Zone diet intentionally distanced themselves from Atkins and the term ‘low carb’ because of the controversies, though their recommendations were based on largely the same principles .[38][39] It can be controversial which diets are low-carbohydrate and which are not.[citation needed] The 1990s and 2000s saw the publication of an increased number of clinical studies regarding the effectiveness and safety (pro and con) of low-carbohydrate diets (see low-carbohydrate diet medical research).

In the United States, the diet has continued to garner attention in the medical and nutritional science communities, and also inspired a number of hybrid diets that include traditional calorie-counting and exercise regimens.[7][40][41][42] Other low-carb diets, such as the Paleo Diet, focus on the removal of certain foods from the diet, such as sugar and grain.[43] On September 2, 2014 a small randomized trial by the NIH of 148 men and women comparing a low-carbohydrate diet with a low fat diet without calorie restrictions over one year showed that participants in the low-carbohydrate diet had greater weight loss than those on the low-fat diet.[44] The low-fat group lost weight, but appeared to lose more muscle than fat.[45]

No consensus definition exists of what precisely constitutes a low-carbohydrate diet.[46] Medical researchers and diet advocates may define different levels of carbohydrate intake when specifying low-carbohydrate diets.[46][not in citation given]

The American Academy of Family Physicians defines low-carbohydrate diets as diets that restrict carbohydrate intake to 20 to 60 grams per day, typically less than 20% of caloric intake.[47]

The body of research underpinning low-carbohydrate diets has grown significantly in the decades of the 1990s and 2000s.[48][49] Most research centers on the relationship between carbohydrate intake and blood sugar levels (i.e., blood glucose), as well as the two primary hormones produced in the pancreas, that regulate the blood sugar level, insulin, which lowers it, and glucagon, which raises it.[50]

Low-carbohydrate diets in general recommend reducing nutritive carbohydrates, commonly referred to as “net carbs”, i.e., grams of total carbohydrates reduced by the non-nutritive carbohydrates[51][52] to very low levels. This means sharply reducing consumption of desserts, breads, pastas, potatoes, rice, and other sweet or starchy foods. Some recommend levels less than 20g of “net carbs” per day, at least in the early stages of dieting[53] (for comparison, a single slice of white bread typically contains 15g of carbohydrate, almost entirely starch). By contrast, the U.S. Institute of Medicine recommends a minimum intake of 130g of carbohydrate per day.[54] The FAO and WHO similarly recommend that the majority of dietary energy come from carbohydrates.[55][56]

Although low-carbohydrate diets are most commonly discussed as a weight-loss approach, some experts have proposed using low-carbohydrate diets to mitigate or prevent diseases, including diabetes, metabolic disease, and epilepsy.[57][58] Some low-carbohydrate proponents and others argue that the rise in carbohydrate consumption, especially refined carbohydrates, caused the epidemic levels of many diseases in modern society, including metabolic disease and type 2 diabetes.[59][60][61][62]

A category of diets is known as low-glycemic-index diets (low-GI diets) or low-glycemic-load diets (low-GL diets), in particular the Low GI Diet.[63] In reality, low-carbohydrate diets can also be low-GL diets (and vice versa) depending on the carbohydrates in a particular diet. In practice, though, “low-GI”/”low-GL” diets differ from “low-carb” diets in the following ways: First, low-carbohydrate diets treat all nutritive carbohydrates as having the same effect on metabolism, and generally assume their effect is predictable. Low-GI/low-GL diets are based on the measured change in blood glucose levels in various carbohydrates these vary markedly in laboratory studies. The differences are due to poorly understood digestive differences between foods. However, as foods influence digestion in complex ways (e.g., both protein and fat delay absorption of glucose from carbohydrates eaten at the same time) it is difficult to even approximate the glycemic effect (e.g., over time or even in total in some cases) of a particular meal.[64]

The low-insulin-index diet, is similar, except it is based on measurements of direct insulemic responses i.e., the amount of insulin in the bloodstream to food rather than glycemic response the amount of glucose in the bloodstream. Although such diet recommendations mostly involve lowering nutritive carbohydrates, some low-carbohydrate foods are discouraged, as well (e.g., beef).[65] Insulin secretion is stimulated (though less strongly) by other dietary intake. Like glycemic-index diets, predicting the insulin secretion from any particular meal is difficult, due to assorted digestive interactions and so differing effects on insulin release.[citation needed]

At the heart of the debate about most low-carbohydrate diets are fundamental questions about what is a ‘normal’ diet and how the human body is supposed to operate. These questions can be outlined as follows.

The diets of most people in modern Western nations, especially the United States, contain large amounts of starches, including refined flours, and substantial amounts of sugars, including fructose. Most Westerners seldom exhaust stored glycogen supplies and rarely go into ketosis. This has been regarded by the majority of the medical community in the last century as normal for humans.[citation needed] Ketosis should not be confused with ketoacidosis, a dangerous and extreme ketotic condition associated with type I diabetes. Some in the medical community have regarded ketosis as harmful and potentially life-threatening, believing it unnecessarily stresses the liver and causes destruction of muscle tissues.[citation needed] A perception developed that getting energy chiefly from dietary protein rather than carbohydrates causes liver damage and that getting energy chiefly from dietary fats rather than carbohydrates causes heart disease and other health problems. This view is still held by the majority of those in the medical and nutritional science communities.[66][67][68] However, it is now widely recognized that periodic ketosis is normal, and that ketosis provides a number of benefits, including neuroprotection against diverse types of cellular injury.[69]

People critical of low-carbohydrate diets cite hypoglycemia and ketoacidosis as risk factors. While mild acidosis may be a side effect when beginning a ketogenic diet,[70][71] no known health emergencies have been recorded. It should not be conflated with diabetic ketoacidosis, which can be life-threatening.

A diet very low in starches and sugars induces several adaptive responses. Low blood glucose causes the pancreas to produce glucagon,[72] which stimulates the liver to convert stored glycogen into glucose and release it into the blood. When liver glycogen stores are exhausted, the body starts using fatty acids instead of glucose. The brain cannot use fatty acids for energy, and instead uses ketones produced from fatty acids by the liver. By using fatty acids and ketones as energy sources, supplemented by conversion of proteins to glucose (gluconeogenesis), the body can maintain normal levels of blood glucose without dietary carbohydrates.

Most advocates of low-carbohydrate diets, such as the Atkins diet, argue that the human body is adapted to function primarily in ketosis.[73][74] They argue that high insulin levels can cause many health problems, most significantly fat storage and weight gain. They argue that the purported dangers of ketosis are unsubstantiated (some of the arguments against ketosis result from confusion between ketosis and ketoacidosis, which is a mostly diabetic condition unrelated to dieting or low-carbohydrate intake).[75] They also argue that fat in the diet only contributes to heart disease in the presence of high insulin levels and that if the diet is instead adjusted to induce ketosis, fat and cholesterol in the diet are beneficial. Most low-carb diet plans discourage consumption of trans fat.

On a high-carbohydrate diet, glucose is used by cells in the body for the energy needed for their basic functions, and about two-thirds of body cells require insulin to use glucose. Excessive amounts of blood glucose are thought to be a primary cause of the complications of diabetes, when glucose reacts with body proteins (resulting in glycosolated proteins) and change their behavior. Perhaps for this reason, the amount of glucose tightly maintained in the blood is quite low. Unless a meal is very low in starches and sugars, blood glucose will rise for a period of an hour or two after a meal. When this occurs, beta cells in the pancreas release insulin to cause uptake of glucose into cells. In liver and muscle cells, more glucose is taken in than is needed and stored as glycogen (once called ‘animal starch’).[76] Diets with a high starch/sugar content, therefore, cause release of more insulin, and so more cell absorption. In diabetics, glucose levels vary in time with meals and vary a little more as a result of high-carbohydrate meals. In nondiabetics, blood-sugar levels are restored to normal levels within an hour or two, regardless of the content of a meal.

However, the ability of the body to store glycogen is finite. Once liver and muscular stores are full to the maximum, adipose tissue (subcutaneous and visceral fat stores) becomes the site of sugar storage in the form of fat.[citation needed] The body’s ability to store fat is almost limitless, hence the modern dilemma of morbid obesity.

While any diet devoid of essential fatty acids (EFAs) and essential amino acids (EAAs) will result in eventual death, a diet completely without carbohydrates can be maintained indefinitely because triglycerides (which make up fat stored in the body and dietary fat) include a (glycerol) molecule which the body can easily convert to glucose.[77] It should be noted that the EFAs and all amino acids are structural building blocks, not inherent fuel for energy. However, a very-low-carbohydrate diet (less than 20 g per day) may negatively affect certain biomarkers[78] and produce detrimental effects in certain types of individuals (for instance, those with kidney problems). The opposite is also true; for instance, clinical experience suggests very-low-carbohydrate diets for patients with metabolic syndrome.[79]

Because of the substantial controversy regarding low-carbohydrate diets and even disagreements in interpreting the results of specific studies, it is difficult to objectively summarize the research in a way that reflects scientific consensus.[80] Although some research has been done throughout the 20th century,[81] most directly relevant scientific studies have occurred in the 1990s and early 2000s. Researchers and other experts have published articles and studies that run the gamut from promoting the safety and efficacy of these diets[82][83] to questioning their long-term validity[84][85] to outright condemning them as dangerous.[86][87] A significant criticism of the diet trend was that no studies evaluated the effects of the diets beyond a few months. However, studies emerged which evaluate these diets over much longer periods, controlled studies as long as two years and survey studies as long as two decades.[82][88][89][90][91]

A systematic review published in 2014 included 19 trials with a total of 3,209 overweight and obese participants, some with diabetes. The review included both extreme low carbohydrate diets high in both protein and fat, as well as less extreme low carbohydrate diets that are high in protein but with recommended intakes of fat. The authors found that when the amount of energy (kilojoules/calories) consumed by people following the low carbohydrate and balanced diets (45 to 65% of total energy from carbohydrates, 25 to 35% from fat, and 10 to 20% from protein) was similar, there was no difference in weight loss after 3 to 6 months and after 1 to 2 years in those with and without diabetes. For blood pressure, cholesterol levels and diabetes markers there was also no difference detected between the low carbohydrate and the balanced diets. The follow-up of these trials was no longer than two years, which is too short to provide an adequate picture of the long term risk of following a low carbohydrate diet.[5]

A 2003 meta-analysis that included randomized controlled trials found that “low-carbohydrate, non-energy-restricted diets appear to be at least as effective as low-fat, energy-restricted diets in inducing weight loss for up to one year.”[92][93][94] A 2007 JAMA study comparing the effectiveness of the Atkins low-carb diet to several other popular diets concluded, “In this study, premenopausal overweight and obese women assigned to follow the Atkins diet, which had the lowest carbohydrate intake, lost more weight and experienced more favorable overall metabolic effects at 12 months than women assigned to follow the Zone, Ornish, or LEARN diets.”[89] A July 2009 study of existing dietary habits associated a low-carbohydrate diet with obesity, although the study drew no explicit conclusion regarding the cause: whether the diet resulted in the obesity or the obesity motivated people to adopt the diet.[95] A 2013 meta-analysis that included only randomized controlled trials with one year or more of follow-up found, “Individuals assigned to a very low carbohydrate ketogenic diet achieve a greater weight loss than those assigned to a low fat diet in the long term.”[96] In 2013, after reviewing 16,000 studies, Sweden’s Council on Health Technology Assessment concluded low-carbohydrate diets are more effective as a means to reduce weight than low-fat diets, over a short period of time (six months or less). However, the agency also concluded, over a longer span (1224 months), no differences occur in effects on weight between strict or moderate low-carb diets, low-fat diets, diets high in protein, Mediterranean diet, or diets aiming at low glycemic indices.[97]

In one theory, one of the reasons people lose weight on low-carbohydrate diets is related to the phenomenon of spontaneous reduction in food intake.[98]

Carbohydrate restriction may help prevent obesity and type 2 diabetes,[99][100] as well as atherosclerosis.[101]

Potential favorable changes in triglyceride and high-density lipoprotein cholesterol values should be weighed against potential unfavorable changes in low-density lipoprotein cholesterol and total cholesterol values when low-carbohydrate diets to induce weight loss are considered.[102] However, the type of LDL cholesterol should also be taken into account here, as it could be that small, dense LDL is decreased and larger LDL molecules are increased with low-carb diets.[citation needed] The health effects of the different molecules are still being elucidated, and many cholesterol tests do not account for such details, but small, dense LDL is thought to be problematic and large LDL is not. A 2008 systematic review of randomized controlled studies that compared low-carbohydrate diets to low-fat/low-calorie diets found the measurements of weight, HDL cholesterol, triglyceride levels, and systolic blood pressure were significantly better in groups that followed low-carbohydrate diets. The authors of this review also found a higher rate of attrition in groups with low-fat diets, and concluded, “evidence from this systematic review demonstrates that low-carbohydrate/high-protein diets are more effective at six months and are as effective, if not more, as low-fat diets in reducing weight and cardiovascular disease risk up to one year”, but they also called for more long-term studies.[103]

A study of more than 100,000 people over more than 20 years within the Nurses’ Health Study observationally concluded a low-carbohydrate diet high in vegetables, with a large proportion of proteins and oils coming from plant sources, decreases mortality with a hazard ratio of 0.8.[104] In contrast, a low-carbohydrate diet with largely animal sources of protein and fat increases mortality, with a hazard ratio of 1.1.[104] This study, however, has been met with criticism, due to the unreliability of the self-administered food frequency questionnaire, as compared to food journaling,[105] as well as classifying “low-carbohydrate” diets based on comparisons to the group as a whole (decile method) rather than surveying dieters following established low-carb dietary guidelines like the Atkins or Paleo diets.[106]

Opinions regarding low-carbohydrate diets vary throughout the medical and nutritional science communities, yet government bodies, and medical and nutritional associations, have generally opposed this nutritional regimen.[citation needed] Since 2003, some organizations have gradually begun to relax their opposition to the point of cautious support for low-carbohydrate diets. Some of these organizations receive funding from the food industry.[citation needed] Official statements from some organizations:

The AAFP released a ‘discussion paper’ on the Atkins diet in 2006. The paper expresses reservations about the Atkins plan, but acknowledges it as a legitimate weight-loss approach.[107]

The ADA revised its Nutrition Recommendations and Interventions for Diabetes in 2008 to acknowledge low-carbohydrate diets as a legitimate weight-loss plan.[108][109] The recommendations fall short of endorsing low-carbohydrate diets as a long-term health plan, and do not give any preference to these diets. Nevertheless, this is perhaps the first statement of support, albeit for the short term, by a medical organization.[110][111] In its 2009 publication of Clinical Practice Recommendations, the ADA again reaffirmed its acceptance of carbohydrate-controlled diets as an effective treatment for short-term (up to one year) weight loss among obese people suffering from type two diabetes.[112]

As of 2003 in commenting on a study in the Journal of the American Medical Association, a spokesperson for the American Dietetic Association reiterated the association’s belief that “there is no magic bullet to safe and healthful weight loss.”[113] The Association specifically endorses the high-carbohydrate diet recommended by the National Academy of Sciences. They have stated “Calories cause weight gain. Excess calories from carbohydrates are not any more fattening than calories from other sources. Despite the claims of low-carb diets, a high-carbohydrate diet does not promote fat storage by enhancing insulin resistance.”[114][bettersourceneeded]

As of 2008[update] the AHA states categorically that it “doesn’t recommend high-protein diets.”[115] A science advisory from the association further states the association’s belief that these diets “may be associated with increased risk for coronary heart disease.”[34] The AHA has been one of the most adamant opponents of low-carbohydrate diets.[citation needed] Dr. Robert Eckel, past president, noted that a low-carbohydrate diet could potentially meet AHA guidelines if it conformed to the AHA guidelines for low fat content.[116]

The position statement by the Heart Foundation regarding low-carbohydrate diets states, “the Heart Foundation does not support the adoption of VLCARB diets for weight loss.”[46] Although the statement recommends against use of low-carbohydrate diets, it explains their major concern is saturated fats as opposed to carbohydrate restriction and protein. Moreover, other statements suggest their position might be re-evaluated in the event of more evidence from longer-term studies.

The consumer advice statements of the NHS regarding low-carbohydrate diets state that “eating a high-fat diet could increase your risk of heart disease” and “try to ensure starchy foods make up about a third of your diet”[117]

In 2008, the Socialstyrelsen in Sweden altered its standing regarding low-carbohydrate diets.[118] Although formal endorsement of this regimen has not yet appeared, the government has given its formal approval for using carbohydrate-controlled diets for medically supervised weight loss.

In a recommendation for diets suitable for diabetes patients published in 2011 a moderate low-carb option (3040%) is suggested.[119]

The HHS issues consumer guidelines for maintaining heart health which state regarding low-carbohydrate diets that “they’re not the route to healthy, long-term weight management.”[120]

Low-carbohydrate diets became a major weight loss and health maintenance trend during the late 1990s and early 2000s.[121][122][123] While their popularity has waned recently from its peak, they remain popular.[124][125] This diet trend has stirred major controversies in the medical and nutritional sciences communities and, as yet, there is not a general consensus on their efficacy or safety.[126][127] Many in the medical community remain generally opposed to these diets for long term health[128] although there has been a recent softening of this opposition by some organizations.[129][130]

Because of the substantial controversy regarding low-carbohydrate diets, and even disagreements in interpreting the results of specific studies, it is difficult to objectively summarize the research in a way that reflects scientific consensus.[131][132][133]

Although there has been some research done throughout the twentieth century, most directly relevant scientific studies have occurred in the 1990s and early 2000s and, as such, are relatively new and the results are still debated in the medical community.[132] Supporters and opponents of low-carbohydrate diets frequently cite many articles (sometimes the same articles) as supporting their positions.[134][135][136] One of the fundamental criticisms of those who advocate the low-carbohydrate diets has been the lack of long-term studies evaluating their health risks.[137][138] This has begun to change as longer term studies are emerging.[82]

A 2012 systematic review studying the effects of low-carbohydrate diet on weight loss and cardiovascular risk factors showed the LCD to be associated with significant decreases in body weight, body mass index, abdominal circumference, blood pressure, triglycerides, fasting blood sugar, blood insulin and plasma C-reactive protein, as well as an increase in high-density lipoprotein cholesterol (HDL). Low-density lipoprotein cholesterol (LDL) and creatinine did not change significantly. The study found the LCD was shown to have favorable effects on body weight and major cardiovascular risk factors (but concluded the effects on long-term health are unknown). The study did not compare health benefits of LCD to low-fat diets.[139]

A meta-analysis published in the American Journal of Clinical Nutrition in 2013 compared low-carbohydrate, Mediterranean, vegan, vegetarian, low-glycemic index, high-fiber, and high-protein diets with control diets. The researchers concluded that low-carbohydrate, Mediterranean, low-glycemic index, and high-protein diets are effective in improving markers of risk for cardiovascular disease and diabetes.[140]

In the first week or two of a low-carbohydrate diet, much of the weight loss comes from eliminating water retained in the body.[141] The presence of insulin in the blood fosters the formation of glycogen stores in the body, and glycogen is bound with water, which is released when insulin and blood sugar drop.[citation needed][142] A ketogenic diet is known to cause dehydration as an early, temporary side-effect.[143]

Advocates of low-carbohydrate diets generally dispute any suggestion that such diets cause weakness or exhaustion (except in the first few weeks as the body adjusts), and indeed most highly recommend exercise as part of a healthy lifestyle.[142][144] A large body of evidence stretching back to the 1880s shows that physical performance is not negatively affected by ketogenic diets once a person has been accustomed to such a diet.[145]

Arctic cultures, such as the Inuit, were found to lead physically demanding lives consuming a diet of about 1520% of their calories from carbohydrates, largely in the form of glycogen from the raw meat they consumed.[145][146][147][148] However, studies also indicate that while low-carb diets will not reduce endurance performance after adapting, they will probably deteriorate anaerobic performance such as strength-training or sprint-running because these processes rely on glycogen for fuel.[144]

Many critics argue that low-carbohydrate diets inherently require minimizing vegetable and fruit consumption, which in turn robs the body of important nutrients.[149] Some critics imply or explicitly argue that vegetables and fruits are inherently all heavily concentrated sources of carbohydrates (so much so that some sources treat the words ‘vegetable’ and ‘carbohydrate’ as synonymous).[150] While some fruits may contain relatively high concentrations of sugar, most are largely water and not particularly calorie-dense. Thus, in absolute terms, even sweet fruits and berries do not represent a significant source of carbohydrates in their natural form, and also typically contain a good deal of fiber which attenuates the absorption of sugar in the gut.[151] Lastly, most of the sugar in fruit is fructose, which has a reported negligible effect on insulin levels in obese subjects.[152]

Most vegetables are low- or moderate-carbohydrate foods (in the context of these diets, fiber is excluded because it is not a nutritive carbohydrate). Some vegetables, such as potatoes and carrots, have high concentrations of starch, as do corn and rice. Most low-carbohydrate diet plans accommodate vegetables such as broccoli, spinach, cauliflower, and peppers.[153] The Atkins diet recommends that most dietary carbs come from vegetables. Nevertheless, debate remains as to whether restricting even just high-carbohydrate fruits, vegetables, and grains is truly healthy.[154]

Contrary to the recommendations of most low-carbohydrate diet guides, some individuals may choose to avoid vegetables altogether to minimize carbohydrate intake. Low-carbohydrate vegetarianism is also practiced.

Raw fruits and vegetables are packed with an array of other protective chemicals, such as vitamins, flavonoids, and sugar alcohols. Some of those molecules help safeguard against the over-absorption of sugars in the human digestive system.[155][156] Industrial food raffination depletes some of those beneficial molecules to various degrees, including almost total removal in many cases.[157]

The major low-carbohydrate diet guides generally recommend multivitamin and mineral supplements as part of the diet regimen, which may lead some to believe these diets are nutritionally deficient. The primary reason for this recommendation is that if the switch from a high-carbohydrate to a low-carbohydrate, ketogenic diet is rapid, the body can temporarily go through a period of adjustment during which it may require extra vitamins and minerals. This is because the body releases excess fluids stored during high-carbohydrate eating. In other words, the body goes through a temporary “shock” if the diet is changed to low-carbohydrate quickly, just as it would changing to a high-carbohydrate diet quickly. This does not, in and of itself, indicate that either type of diet is nutritionally deficient. While many foods rich in carbohydrates are also rich in vitamins and minerals, many low-carbohydrate foods are similarly rich in vitamins and minerals.[158]

A common argument in favor of high-carbohydrate diets is that most carbohydrates break down readily into glucose in the bloodstream, and therefore the body does not have to work as hard to get its energy in a high-carbohydrate diet as a low-carbohydrate diet. This argument, by itself, is incomplete. Although many dietary carbohydrates do break down into glucose, most of that glucose does not remain in the bloodstream for long. Its presence stimulates the beta cells in the pancreas to release insulin, which has the effect of causing about two-thirds of body cells to take in glucose, and causing fat cells to take in fatty acids and store them. As the blood-glucose level falls, the amount of insulin released is reduced; the entire process is completed in non-diabetics in an hour or two after eating.[citation needed] High-carbohydrate diets require more insulin production and release than low-carbohydrate diets,[citation needed] and some evidence indicates the increasingly large percentage of calories consumed as refined carbohydrates is positively correlated with the increased incidence of metabolic disorders such as type 2 diabetes.[159]

In addition, this claim neglects the nature of the carbohydrates ingested. Some are indigestible in humans (e.g., cellulose), some are poorly digested in humans (e.g., the amylose starch variant), and some require considerable processing to be converted to absorbable forms. In general, uncooked or unprocessed (e.g., milling, crushing, etc.) foods are harder (typically much harder) to absorb, so do not raise glucose levels as much as might be expected from the proportion of carbohydrate present. Cooking (especially moist cooking above the temperature necessary to expand starch granules) and mechanical processing both considerably raise the amount of absorbable carbohydrate and reduce the digestive effort required.

Analyses which neglect these factors are misleading and will not result in a working diet, or at least one which works as intended. In fact, some evidence indicates the human brain the largest consumer of glucose in the body can operate more efficiently on ketones (as efficiency of source of energy per unit oxygen).[160]

The restriction of starchy plants, by definition, severely limits the dietary intake of microbiota accessible carbohydrates (MACs) and may negatively affect the microbiome in ways that contribute to disease.[161] Starchy plants, in particular, are a main source of resistant starch an important dietary fiber with strong prebiotic properties.[162][163][164] Resistant starches are not digestible by mammals and are fermented and metabolized by gut flora into short chain fatty acids, which are well known to offer a wide range of health benefits.[163][165][166][167][168][169] Resistant starch consumption has been shown to improve intestinal/colonic health, blood sugar, glucose tolerance, insulin-sensitivity and satiety.[170][171][172] Public health authorities and food organizations such as the Food and Agricultural Organization, the World Health Organization,[173] the British Nutrition Foundation[174] and the U.S. National Academy of Sciences[175] recognize resistant starch as a beneficial carbohydrate. The Joint Food and Agricultural Organization of the United Nations/World Health Organization Expert Consultation on Human Nutrition stated, “One of the major developments in our understanding of the importance of carbohydrates for health in the past twenty years has been the discovery of resistant starch.”[173]

In 2004, the Canadian government ruled that foods sold in Canada could not be marketed with reduced or eliminated carbohydrate content as a selling point, because reduced carbohydrate content was not determined to be a health benefit. The government ruled that existing “low carb” and “no carb” packaging would have to be phased out by 2006.[176]

Some variants of low-carbohydrate diets involve substantially lowered intake of dietary fiber, which can result in constipation if not supplemented.[citation needed] For example, this has been a criticism of the induction phase of the Atkins diet (the Atkins diet is now clearer about recommending a fiber supplement during induction). Most advocates[who?][dubious discuss] today argue that fiber is a “good” carbohydrate and encourage a high-fiber diet.[citation needed]

Low-carbohydrate diet – Wikipedia

Feline Obesity: An Epidemic of Fat Cats

06-12-2016 11:46 pm

Lisa A. Pierson, DVM

French translation

When was the last time you saw an obese lion? How about a chubby cheetah? Or a fat tiger? Have you ever seen an overweight leopard or panther? If you have ever watched nature programs on TV, I am sure that you know the answer to the questions just posed.

The answer is never.

The next questions are also easy ones to answer even if you are like me and turn your head when scenes of wild carnivores eating their prey pop up on the television screen!

Do these wild cats eat a dry food diet that is full of starchy carbohydrates in the form of grains? Do they eat a water-depleted diet in the form of dry kibble? Is their diet one that derives much of its protein from plants (versus meat) as is true of many dry food diets?

The answers are, again, simple: no, no, and no.

There was a wonderful program on the TLC channel a few years ago entitledHoney Were Killing the Kids. This program addressed the obesity epidemic in this country starting with what we are feeding to our children. Americans are eating themselves right into an early grave but that is their choice. Our cats, on the other hand, do not have a choice and are stuck with whatever their human caregiver decides to put on their dinner plate and we owe it to them to feed a healthy diet.

This webpage could be aptly named Honey, Were Killing our Pets.

If you have not read my article entitled Feeding Your Cat: Know the Basics of Feline Nutrition, I urge you to do so now and then come back to this page. In order for you to understand how to tackle feline obesity, you must first understand how to properly feed a cat. After all, cats, like humans, do not become obese if they are eating a healthy, species-appropriate diet with their caloric intake properly balanced with their caloric expenditure.

Please note that I used the word healthy in the above statement. People and animals can, indeed, maintain an appropriate weight even when eating anunhealthy diet. So, to that end, it is very important to understand that even if you have a cat that is at an appropriate weight, this does not necessarily mean that he is eating a healthy diet.

As outlined in my Feeding Your Cat article, your cat has a much better chance of optimal health if he is fed a canned food diet instead of dry kibble.

Dry food is not a healthy diet for any cat because it is:

Please click on the links below to read more about the key issues associated with feline obesity.

Why are there so many fat cats?

How to evaluate your own cats weight

We owe it to our cats to feed them properly

Recognizing fat versus muscle

Implementing a safe weight-loss program

How fast should my cat lose weight?

How much should I feed?

Consider calories, not just ounces

Multiple cat households

Mistake made with Bennie protein malnourishment

Case study Molly

Case study Bennie

Type of diet dry kibble

Obligate carnivores are designed to meet their energy needs with calories supplied by protein and fat not by carbohydrates. The average prey (birds, mice, rabbits, etc.) of a wild cat is made up of only 3 5% of calories from carbohydrates. Now consider that dry kibble diets generally range from 35% 50% carbohydrate calories and you will see a serious disconnect between what the cat is designed to eat and what Man insists on feeding to them. Dry foods flood the cats system with 5-10 times (500% 1,000%) more calories from carbohydrates than what would be found in a wild cats prey.

According to Dr. Zorans paper The Carnivore Connection to Nutrition in Cats, carbohydrates are minimally used for energy by the cat and those that are not used are converted to, and stored as, fat. The so-called light diets that are on the market have targeted the fat content as the nutrient to be decreased but, in doing so, the pet food manufacturers have increased the grain fraction (because grains are always cheaper than meat), leading to a higher level of carbohydrates.

Hence, many overweight cats eating these diets are still obese. These light products are among the most species-inappropriate, unhealthy diets available to cat caretakers. Many caretakers feed very small amounts of these diets hoping that their cat will lose weight but feeding a small amount of a diet that is inappropriate for the species is not the answer! The caretaker usually just ends up with a crabby cat that is often still overweight.

Why are dry foods so high in carbohydrates? Think profit margin. Grains are cheap. Meat is expensive.

Why are dry foods so popular? Because they are cheap and convenient.

Our cats are a captive audience. They depend on us, with our opposable thumbs and the common sense part of our brains engaged, to feed them a diet that promotes health one that they would be eating if left to their own devices in a natural setting not one that is just cheap and convenient.

Important note: Feeding the least expensive canned food is far better than feeding the most expensive dry food. When considering the issue of obesity, consider that dry food is only 10% water and canned food is 78% water. Therefore, dry foods are more calorie-densethan canned food.

Method of feeding

Another very significant issue contributing to the obesity epidemic is the method in which dry food is often fed. Many people free-feed their cats. However, think about what your human childs waistline would look like if you put out a bowl of very palatable high carb food for them to eat whenever they wanted to!

Some cats will properly regulate their intake when dry food is free-fed but many will not.

There are three main reasons why cats tend to overeat when free-fed high carb dry food. The first reason is because the pet food manufacturers do not play fair when manufacturing dry food. They coat the kibble with extremely enticing animal digests which makes this inferior source of food very palatable to the target animal. (Think about the last time you sat down with a very tasty meal or snack. Did you eat well past the point that your stomach was satisfied in terms of fullness? We all keep eating when we shouldnt.simply because it tastes good.)

The second reason that some cats tend to consume too many calories when eating dry food is because an obligate carnivore is designed to be satiated when he has consumed an adequate amount of protein and fat. Carbohydrates do not seem to send the Im full and can now stop eating signal to a cats brain like protein and fat do.

The third reason why some cats overeat is boredom. This is especially true for indoor-only cats.

Of course there are many cats that are free-fed high carb dry food that do not gain an excessive amount of weight. This variability exists in the human population also. Some living beings are simply more food-oriented than others. Unfortunately, even these cats regardless of their weight are still being fed an unhealthy diet.

Activity level

An indoor-only cat will usually not burn off as many calories as an outdoor cat. Also, as mentioned above, indoor cats often eat out of boredom (just like humans) and end up overweight. Of course, the safest place for a cat is indoors but just because a cat lives its life inside, this does not mean that he has to be overweight.

Interact with your cat as much as possible using tassel toys, etc. This will not only burn off calories but will also alleviate boredom. Many people use laser lights but I always feel sorry for the cat since they are never able to actually catch their prey! Some people hide small bowls of canned food around the house to make their cats roam around looking for their prey meal.

Here is a video of Bennie running back and forth in chasing 20-25 pieces of dry food (EVO grain-free) that he is getting as a treat. This game allows for 20-25 calories out of his 180 calorie daily allotment.

Please do not fall for the marketing gimmick of the Indoor Cat formulas of food. Cats did not suddenly stop being obligate carnivores just because they stepped inside under a roof. These diets often have an atrocious list of ingredients and are usually loaded with high carb grains.

Here are two pictures of a cat that, on the outside, appeared to be at an acceptable weight even on the thin side. He was being fed a high carbohydrate dry food diet and you can see what his insides looked like. All of the light colored tissue is fat. There is so much fat inside of this cat that his kidneys (oval, pink organs) are barely visible. Some of you may also have heard of omental fat that human nutritionists and doctors talk about when discussing risk factors for death in overweight humans. On the left side of the top picture and the right side of the bottom picture you will see omental fat.

Right kidney surrounded by fat

Left Kidney engulfed in fat

You may be wondering if your cat really is overweight. Generally speaking, I find that humans tend to think that a chubby cat is cute and healthy when, in reality, the cat is carrying around too much fat.

Note that you should be able to easily feel the ribs with just a slight fat pad over them. Cats should also have a waist when viewed from above. They should not have any fat pads over their shoulders and if you pick up their skin, you should not feel thick fat underneath.

Their top line (backbone and back of the head) should be well-muscled and not terribly prominent (too thin) or hard to feel (too fat).

The top line is the preferred area to assess/monitor during a weight loss program or as the cat ages. This part of the body gives a very good indication of the overall body weight/condition of the cat.

Important note: I do not consider loose skin on the underside of the cats abdomen to be a sign of being overweight. Many cats (males and females) have this doolap and if it is just loose skin and not fat this is nothing to be concerned about. (My Amber sporting her new lion cut hairdo gave me permission to post her doolap for the world to see. She is well-muscled and not overweight.but could use a tummy tuck.)

The feeding of dry food plays a very significant role in many of the diseases that plague our cats including obesity, diabetes, urinary tract problems, and inflammatory bowel disease.

See Feline Urinary Tract Health for a discussion of how a water-depleted diet causes a great deal of suffering in our cats.

Regarding feline diabetes, the links between dry food and this serious disease are two-fold:

Most people are familiar with the Atkins diet which is based on a high protein/moderate fat/low carbohydrate calorie distribution. Personally, I think that this diet is a bit extreme for humans since we are designed to consume carbohydrates in the form of vegetables and whole grains. However, the cat is definitely designed to eat an Atkins-type of diet due to their metabolic make up that defines them as obligate carnivores.

This status is reflected by their lack of enzymatic pathways to efficiently utilize high levels of dietary carbohydrates. This is why the feline species-appropriate diet is often referred to as the Catkins Diet.

It is important to understand the basic three elements of food/calories:

It is best to list foods in terms of caloric composition which reflects the percentage of total calories that come from protein, fat, and carbohydrate. The caloric breakdown of these three nutrient classes must add up to 100% of total calories. Therefore, if one class of nutrient is decreased, one, or both, of the other two must increase.

*A very important note about protein: Not all proteins are created equal. Proteins can either be from animals or plants. What defines cats as obligate (strict) carnivores is their need to consume protein from other animals not plants.

Protein derived from animal tissues has a complete amino acid profile. (Amino acids are the building blocks of proteins. Think of them as pieces of a puzzle.) Plant-based protein does not contain the full compliment (puzzle pieces) of the critical amino acids required by an obligate carnivore. The quality and composition of a protein (are all of the puzzle pieces present?) is also referred to as its biological value.

Humans and dogs can take the pieces of the puzzle in the plant protein and, from those, make the missing pieces. Cats cannot do this. This is why humans and dogs can live on a vegetarian diet but cats cannot. (Note that I do not recommend vegetarian diets for dogs.)

Grains (corn, wheat, soy, rice, etc.) are made up of proteins (plant-based poor biological value) and carbohydrates.

Most dry foods are heavily grain-based but it is important to recognize that pet food companies are sneaky. Many of them put grain-free on the label but then fill up the food (and increase their profit margin) with peas and potatoes which are high in carbohydrates and are plant-based protein sources but are not technically grains.

Because the protein in dry food is often heavily plant-based, the overall protein content in this type of food earns a lower biological value score when compared to the protein in canned foods which is usually animal (meat)-based.

And, the grains/potatoes/peas in dry food also contribute a high carbohydrate load to your obligate carnivores body.

Because plant proteins are cheaper than meat proteins, pet food companies will have a higher profit margin when using these ingredients.

Dry food addicts: Unfortunately, many cats have been fed dry food for their entire lives. It is no wonder that they are conditioned to eat this unhealthy diet. If I had a dime for every time I have heard someone say but my cat really.really likes his dry food I would be wealthy.

People like cookies and potato chips but that does not mean that these food items constitute a health diet.

Cats that have grown up on dry food find the consistency of canned food very foreign and often refuse to even give it a try.

My cats had been fed a 100% dry food diet for their entire lives. When I started introducing canned food to them in December of 2002, their ages ranged from 2 to 10 years. They all looked at me like I had rocks for brains..wondering what in the world that wet stuff was in their food bowls. It took a very frustrating, three month-long period of time to get them off of dry food and eating canned food. After transitioning to canned food, I took it one step further. In March of 2003, I transitioned them to a balanced homemade raw or semi-cooked meat diet and I could not be happier with their health.

See Tips for Transitioning Dry Food Addicts to Canned Food.

Low carbohydrate dry foods: There are three dry foods on the market that are lower in carbs than most dry foods but please do not think that these foods are a healthy option to low-carb canned food.

Three lower-carb dry foods on the market are Innova EVO, Wellness CORE, and Young Again. While these foods do address the high carb issue, they are still water-depleted diets that should not be fed to a species that has aninherently low thirst drive. Dry food sets your cat up for serious urinary tract problems.

Cats are designed to obtain water with their food since their normal prey contains approximately 75% water. Dry foods only contain 10% water whereas canned foods contain approximately 78% water. Canned foods therefore more closely approximate the natural diet of the cat and are better suited to meet the cats water needs.

People often say but my cat drinks a lot of water so he must be getting enough!

Because cats have a low thirst drive, they do not make up the hydration deficit at the water bowl when consuming a dry food diet.

It has been shown that cats on canned food when compared to dry food-fed cats consume double the amount of water when all sources (from the food and the water bowl) are considered. This also means that their urine output is increased significantly which promotes urinary tract health by frequently hosing out your cats bladder of crystals and any inflammatory debris.

Please understand that this necessitates more frequently cleaning of their litter box or the addition of more litter boxes in the home. We need to always be respectful of the cats fastidiously clean nature and and have a clean litter box available for them at all times.

In addition to being water-depleted, these grain-free dry foods are high in phosphorus which is not a good mineral to have in abundance especially for senior cats that may have marginal kidney function.

A third and very important issue is that these three dry foods are verycalorie-dense. For instance, dry EVO contains a whopping 612 calories/cup. Most dry foods are ~400 calories/cup or less. Considering that the average 10 pound cat only needs about 200 calories per day to maintain their weight, you can see that 1/3 of a cup of EVO meets these caloric needs yet many people feed far more of this diet than 1/3 of a cup.

Combine a very palatable diet with high caloric density and throw in the fact that many people free-feed their cats dry food and you have a perfect recipe forobesity when these dry foods are fed. You can use these products as transition foods in order to cut the carbs in the diet but you must be very aware that these diets are very calorie dense and a little bit goes a long way. Portion control of these diets is a must!

A fourth issue is that these diets, like all dry foods, are cooked for a very long time at very high temperatures. Many vital nutrients are damaged or destroyed by this harsh cooking process and then Man has to guess which ingredients, and in what form and amount, will need to be added to restore the health of the diet. Man is just not as smart as nature which makes it impossible to know exactly what has been damaged and how to restore the food to an optimal level of nutrition.

Ok..we have discussed the fact that canned food is better for cats than dry food so the question iswhat do we look for in a canned food?

Please see Commercial Food for a more detailed discussion on this subject.

Ideally, for an otherwise healthy cat, we want to feed a high protein/moderate fat/low carbohydrate canned food. In other words, a mouse.

In terms of caloric breakdown that means approximately:

Keep in mind that when you are reading the Cat Food Composition chart, the protein, fat, and, carbohydrate calories (the first three columns) must add up to 100%.

Unfortunately, many commercial cats foods that fit the above criteria contain fish. As is common knowledge, fish can be contaminated with heavy metals such as mercury. Also, research has shown that fire retardant chemicals (PBDEs) are more highly concentrated in fish and there is a strong link between these chemicals and hyperthyroidism. As well, fish is one of the most common hyperallergenic proteins for cats.

When choosing a canned food, think feathers and long ears.iepoultry and rabbit and not so much fish. Fish-based cat foods can be used to help transition dry food addicts to canned food but cats tend to get fixated on it and then will not eat a more suitable diet of poultry or rabbit. Therefore, try to wean your cats off of fish as soon as possible.

Some cats do fine with beef but this protein source also tends to be hyperallergenic in some cats so I recommend staying away from beef if your cat has any gastrointestinal problems such as vomiting or diarrhea.

We have established the fact that canned is better than dry for overall health but.. can a cat get fat on high protein/low-carb canned food?

You bet he can!

Read more here:
Feline Obesity: An Epidemic of Fat Cats

Atkins diet – Wikipedia

06-12-2016 8:41 am

The Atkins diet, also known as the Atkins nutritional approach, is a low-carbohydrate diet promoted by Robert Atkins and inspired by a research paper he read in The Journal of the American Medical Association. The paper entitled “Weight Reduction” was published by Alfred W. Pennington in 1958.[1]

The Atkins diet is classified as a fad diet.[2] There is only weak evidence supporting its effectiveness in helping achieve sustainable weight loss.[3][4]

There is only weak evidence that the Atkins diet is effective in helping people achieve short-term weight loss, or that it is better than not dieting at all in the longer term.[3][4] One review found that the Atkins diet led to 0.1% to 2.9% more weight loss at one year compared to a control group which received behavioural counselling.[3]

Because of substantial controversy regarding the Atkins diet and even disagreements in interpreting the results of specific studies it is difficult to objectively summarize the research in a way that reflects scientific consensus.[5][6] Although there has been some research done throughout the twentieth century,[7][8] most directly relevant scientific studies, both those that directly analyze the Atkins Diet and those that analyze similar diets, have occurred in the 1990s and early 2000s and, as such, are relatively new. Researchers and other experts have published articles and studies that run the gamut from promoting the safety and efficacy of the diet,[9][10] to questioning its long-term validity,[11][12] to outright condemning it as dangerous.[13][14] A significant early criticism of the Atkins Diet was that there were no studies that evaluated the effects of Atkins beyond a few months. However, studies began emerging in the mid-to-late-2000s which evaluate low-carbohydrate diets over much longer periods, controlled studies as long as two years and survey studies as long as two decades.[9][15][16][17]

There is some evidence that adults with epilepsy may benefit from therapeutic ketogenic diets, and that a less strict regimen, such as a modified Atkins diet, is similarly effective.[18]

The Atkins diet is a kind of low-carbohydrate fad diet.[2]

The diet involves limited consumption of carbohydrates to switch the body’s metabolism from metabolizing glucose as energy over to converting stored body fat to energy. This process, called ketosis, begins when insulin levels are low; in normal humans, insulin is lowest when blood glucose levels are low (mostly before eating). Reduced insulin levels induce lipolysis, which consumes fat to produce ketone bodies. On the other hand, caloric carbohydrates (for example, glucose or starch, the latter made of chains of glucose) affect the body by increasing blood sugar after consumption.

In his early books such as Dr Atkins’ New Diet Revolution, Atkins made the controversial argument that the low-carbohydrate diet produces a metabolic advantage because “burning fat takes more calories so you expend more calories”.[19] He cited one study in which he estimated this advantage to be 950 Calories (4.0 MJ) per day. A review study published in Lancet[20] concluded that there was no such metabolic advantage and dieters were simply eating fewer calories due to boredom. Astrup stated, “The monotony and simplicity of the diet could inhibit appetite and food intake.”

In the most recent book by Westman, Phinney, and Volek, the authors suggest optimal levels of protein, fat, and calorie intake, and have moved away from the metabolic advantage theory.

The diet restricts “net carbs” (digestible carbohydrate grams that affect blood sugar less fiber grams). One effect is a tendency to decrease the onset of hunger, perhaps because of longer duration of digestion (fats and proteins take longer to digest than carbohydrates). The 2002 book New Diet Revolution states that hunger is the number one reason that low-fat diets fail, and that the diet is easier because one is satisfied with adequate protein, fat and fiber.[19]

Net carbohydrates can be calculated from a food source by subtracting fiber and sugar alcohols from total carbohydrates. Sugar alcohols contain about two calories per gram, although the American Diabetes Association recommends that diabetics not count alcohol as carbohydrates.[21]Fructose (for example, as found in many industrial sweeteners) has four calories per gram but has a very low glycemic index[22] and does not cause insulin production, probably because cells have low levels of GLUT5.[23][24] Leptin, an appetite-regulating hormone, is not triggered following consumption of fructose. This may for some create an unsatisfying feeling after consumption which might promote binge behavior that culminates in an increased blood triglyceride level arising from fructose conversion by the liver.[25]

Preferred foods in all categories are whole, unprocessed foods with a low glycemic index, although restrictions for low glycemic carbohydrates (black rice, vegetables, etc.) are the same as those for high glycemic carbohydrates (sugar, white bread). Atkins Nutritionals, the company formed to market foods that work with the diet, recommends that no more than 20% of calories eaten while on the diet come from saturated fat.[26]

The Atkins Nutritional Approach gained widespread popularity in 2003 and 2004. At the height of its popularity one in eleven North American adults claimed to be on a low-carb diet such as Atkins.[27] This large following was blamed for large declines in the sales of carbohydrate-heavy foods like pasta and rice: sales were down 8.2 and 4.6 percent, respectively, in 2003. The diet’s success was even blamed for a decline in Krispy Kreme sales.[28] Trying to capitalize on the “low-carb craze,” many companies released special product lines that were low in carbohydrates.

In 2003, Atkins died from a fatal head injury due to a fall on ice,[29] and while he had a history of heart disease, Mrs. Atkins was quoted as stating that the circumstances of his death from an epidural hematoma had nothing to do with his diet or history of viral cardiomyopathy.[29][30]

On July 31, 2005, the Atkins Nutritional company filed for Chapter 11 bankruptcy protection after the percentage of adults on the diet declined to two percent and sales of Atkins brand products fell steeply in the second half of 2004.[31] The company continues to operate and the diet plan remains popular, although it has not regained its former popularity.[citation needed]

An analysis conducted by Forbes magazine found that the sample menu from the Atkins Nutritional Approach is one of the top five in the expense category of ten plans Forbes analyzed. This was due to the inclusion of recipes with some high cost ingredients such as lobster tails which were put in the book to demonstrate the variety of foods which could be consumed on the diet. The analysis showed the median average of the ten diets was approximately 50% higher, and Atkins 80% higher, than the American national average. The Atkins Diet was less expensive than the Jenny Craig diet and more expensive than Weight Watchers.[32]

Low-carbohydrate diets have been the subject of heated debate in medical circles for three decades. They are still controversial and only recently has any serious research supported some aspects of Atkins’ claims, especially for short-term weight-loss (6 months or less). In a comparison study by Dansinger and colleagues (2005), the goal was to compare popular diets like Atkins, Ornish, Weight Watchers, and Zone for the amount of weight lost and a heart disease risk reduction. In the study there were 160 participants and it lasted for 1 year. All the subjects were overweight at baseline, and had an increased risk for cardiac diseases. One of the diets was assigned to each person.[33]

The Atkins Diet group were to eat 20g of CHO (carbohydrate) a day, with a gradual increase toward 50 g daily, but according to the study increased to well over 130g after the second month and up to 190g by the sixth month. At this point, the Atkins Diet group were eating carbohydrates equivalent to the other three groups. The Zone group ate a 403030% diet of carbohydrates, fats and proteins respectively. The Weight Watchers group was to keep the “points” of their food in a determined range, based on their weight. The group that was supposed to represent the Ornish diet ate a diet very unlike the Ornish diet that had been shown to reverse heart disease, taking in 30% of calories from fat rather than the suggested 10%, up to 20 grams of saturated fat a day, and only 15 grams of dietary fiber, indicating that the diet was not based on whole plant foods like the typical Ornish diet. The weight, waist size, blood pressure, and a blood sample were taken, at the beginning, after 2 months, 6 months and 12 months. All four diets resulted in modest weight loss and improvement in several cardiac risk factors, with no significant differences between the diets.[33]

Others in the scientific community also raised questions regarding the efficacy and safety of the diet:

Many people believe that the Atkins Diet promotes eating unlimited amounts of fatty meats and cheeses.[37][38] This was allowed and promoted in early editions of the book. In the newest revision, not written by the now-deceased Atkins, this is not promoted. The Atkins Diet does not impose caloric restriction, or definite limits on proteins, with Atkins saying in his book that this plan is “not a license to gorge,” but rather promotes eating protein until satiated. The director of research and education for Atkins Nutritionals, Collette Heimowitz, has stated that the newer revisions are intended to clarify rather than replace the correct advice in the older books.[26]

“The Atkins Diet was labeled as a high-fat diet,” Westman said in an interview with The New York Times. “We’ve been told over the past 40 years that fat in the diet is bad. Now we know that fat is not bad. What’s happened is that there is a paradigm shift in thinking about carbohydrates, fat and protein and health.”[39]

Atkins Nutritionals, Inc. (ANI) was founded in 1989 by Atkins to promote the sale of Atkins-branded products. Following his death, waning popularity of the diet and a reduction in demand for Atkins products, Atkins Nutritionals, Inc. filed for Chapter 11 bankruptcy protection on July 31, 2005 citing losses of $340 million.[40] The company emerged from bankruptcy on January 10, 2006, introducing “a new business strategy that focuses on providing great-tasting portable foods with a unique nutrition advantage to healthy, active men and women.”[41] Although the marketing focus has changed, the products are still low-carb. It is also stated on the packages the stage of the Atkins Nutritional Approach where they may be used.

Atkins diet – Wikipedia

Weight Management-Topic Overview –

03-12-2016 8:42 pm

What is a healthy weight?

A healthy weight is a weight that lowers your risk for health problems. For most people, body mass index (BMI) and waist size are good ways to tell if they are at a healthy weight.

But reaching a healthy weight isn’t just about reaching a certain number on the scale or a certain BMI. Having healthy eating and exercise habits is very important.

If you want to get to a healthy weight and stay there, healthy lifestyle changes will work better than dieting. Reaching a certain number on the scale is not as important as having a healthy lifestyle.

Staying at a healthy weight is one of the best things you can do for your health. It can help prevent serious health problems, including:

But weight is only one part of your health. Even if you carry some extra weight, eating healthy foods and being more active can help you feel better, have more energy, and lower your risk for disease.

In today’s society, there is a lot of pressure to be thin. But being thin has very little to do with good health. Many of us long to be thin, even though we’re already at a healthy weight. So we get desperate, and we turn to diets for help.

If you decide that you do need to make some changes, here are the three steps to reaching a healthy weight:

One Woman’s Story:

“The biggest key to my success is knowing that this is a process. It’s not ‘all or nothing at all.’ It’s a matter of making choices every day. One day I might decide to eat more than another day, and that’s okay, as long as I’m paying attention. I finally realized it wasn’t a time-limited thing. It became much more of a lifestyle change than a temporary diet. The idea that somehow I could go back to my old ways was just not there anymore.”Maggie

Read more about how Maggie changed her life and lost 50 pounds.

WebMD Medical Reference from Healthwise

Visit link:
Weight Management-Topic Overview –

Fad Diets vs Long-Term Weight Loss – Skinny Ms.

03-12-2016 8:41 pm

Theinternet is filled with all kind of weight loss advice, ranging from simple tips, such as having a glass of water first thing after waking up, to strange fads, such as eating only bananas. With so much conflicting advice, its difficult to distinguish between the good and the bad. Where do you draw the line between what is genuinely helpful for long term weight loss and what is a ridiculous fad?

To make things more complicated, sometimes websites will give advice that results in quick weight loss that is actually harmful to your health in the long term. This includes many detoxes, low-calorie diets, or meal plans that completely eliminate important food groups. When bad weight loss advice can appear effective, how do you find effectivelong term weight loss tips?

Although there is not always a clear distinction, weve put together a list of five key qualities to look for in advice. These 5 differences between a fad diet and long-term weight loss will help you distinguish between tips that will help you lose and keep the pounds off, and tips that can be detrimental to your health.

1. Long term weight loss takes time. The internet is full of short-term diets that promise to make you drop 5 or 10 pounds in a week. What these diets often do is help you de-bloat or help your body clean out waste from your digestive tract. While this approach can give you a flatter stomach quickly, the results wont last. After the first few days, your body will return to its typical water and waste retention, meaning that the excess pounds will return as quickly as they disappeared. It is near impossible to lose this much weight in body fat in just a few days.

It is estimated that a person needs to burn around 3,500 calories in order to lose a pound of fat. In order to lose 5 pounds in one week, you need a deficit of 17,500 calories. This is a deficit of 2,500 calories per day. Keep in mind that this is just the deficit, meaning that you would need to burn whatever you eat on top of those 2,500 calories.

A more reasonable aim for long term weight loss is closer to a 500 calorie deficit per day. The number on the scale will drop slowly, but it will keep dropping instead of springing back up. Instead of following a quick-fix diet, try making small changes to your habits that will help you burn more calories throughout the day. Check out our post on 13 ways to burn extra calories in just 4 minutes a day.

2. Fad diets often eliminate essential nutrients. An example of an extreme diet that eliminates essential nutrients is a meal plan that has you eat nothing but boiled potatoes and baked chicken breast. Even if youre eating in the ideal calorie range, you might not be getting all your vitamins and minerals. A lack of vitamin C and A can weaken your immune system and leave you vulnerable to colds and influenza. A nutrient deficit can also cause amenorrhea, the loss of menstruation, is women. If your body lacks certain nutrients, you might become vulnerable to binges, meaning all weight loss efforts can be undone in a short period of time.

Look for meal plans that allow you to eat a wide variety of fruits and vegetables. Make sure you include sources of lean protein and healthy fats. No major food group should be eliminated. Even making room for the occasional dessert can be more effective for long term weight loss. Our meal planning posts can help you find tons of delicious new recipes that use fruits, veggies, whole grains, and lean protein.

3. Too few calories can actually make you gain weight in the long term. Another way you can become vulnerable to binges is by not eating enough calories. When your body doesnt get enough energy to function properly, it freaks out and sends signals to your brain that you are in dire need of food. This causes you to crave high-calorie treats, often in the form of high-fat, high-sugar combinations such as ice cream, cakes, deep-fried meat, or sauce-drenched chicken wings.

Keeping your body at an elevated calorie deficit for a long period of time can cause permanent damage to your mind and body. Your metabolism will slow down. Non-essential processes will shut down. Muscle mass will decrease much faster than fat stores. Menstruation will stop. Your heart will weaken and you will lose bone density. Studies have also shown the link between starvation and mental deterioration. Depriving your body of necessary calories leaves you vulnerable to eating disorders. You become overly focused on food, even while depriving yourself of it. Hoarding habits, mood swings, and personality shifts have all been linked to starvation.

When following diets and meal plans from the internet, its very important to make sure you are still eating enough to keep your mind and body healthy. Unless advised by a doctor, try to keep your calorie deficit close to the recommended 500 calories per day.

4. Long term weight loss doesnt involve fasting days. Fad diets and detoxes often ask you to fast for a day. They can also ask you to keep your calorie intake extremely low for a day or two. Many people believe that if the fast only lasts for a little while, it doesnt cause any harm and can aid your long-term goals. While a one-day fast might not seem like much, it can still put tremendous stress on your body.

Your body works at its best when it has a steady stream of energy. This is why its often recommended to eat small frequent meals, instead of large meals two or three times a day. Fasting for a day will slow your metabolism and leave you feeling tired and sluggish.

Long term weight loss sets up a routine where you eat the recommended amount of calories every day. Remember to keep your deficit within a reasonable range.

5. Long term weight loss includes carbs, fats, and proteins. Carbs, fats, and protein are known as macronutrients. These are the foundation for healthy eating.

Many fad diets eliminate or severely limit one of these groups. The latest trends tend to cut carbs almost entirely. In the past few years, some have responded to the low-carb trend by preaching a high-carb, low-fat diet instead. In reality, both carbs and fats are important components of a balanced diet. Carbs are the main source of energy for your body. Fats are essential for proper brain function and play an important role in making you feel satiated.

Instead of eliminating or limiting macronutrients, look for a diet thats structured around healthy carbs and fats. This means whole grains instead of added sugar, and fish instead of deep-fried treats.

Sources of healthy carbs include squashes, beans, fruit, oatmeal, and most vegetables. Healthy fats are found in fish, avocados, nuts, and seeds. Browse our recipes to find meals full of nutritional superstars.

To learn more about what makes a healthy diet, check out our posts on weight loss. You can find tons of tips and tricks to lose weight the healthy way!

How do you differentiate between fad diets and long term weight loss? Let us know! Leave a comment in the section below.

Go here to read the rest:
Fad Diets vs Long-Term Weight Loss – Skinny Ms.

Sports Medicine 2017 | Sports Medicine Barcelona | Fitness …

02-12-2016 11:43 am

Market Analysis Report

Importance & Scope:

Health play a vital role for any living being on this earth, nothing can be good, if the health is not good. Healthy and physically fit person can enjoy their lives more beautifully. Sports Medicine is the subjust which deals with all the health and physical related conditions of the athlates. Sports Medicine Conference is the most precious event which is directly related to health and wellness not only for the sports person/athletes but also for the people who are agonize with most of the diseases and disorders which are directly or indirectly related to the physical health and condition. Sports medicine is a towering subject which is related to physical health and conditions.

There is a huge demand for the sports medicine in most of the countries where sports and physical health are given more important. Sports Medicine 2016 aims to bring together leading academic scientists, researchers and research scholars to exchange and share their experiences and research results about all aspects of Sports, Physical Health, Injuries and Medicine. It also provides the chance for researchers, practitioners and educators to present and discuss the most recent innovations, trends, and concerns, practical challenges encountered and the solutions adopted in the fields of Sports Medicine and Fitness.

Sports Medicine2016 is an international platform for presenting research about marketing, exchanging ideas about it and thus, contributes to the dissemination of knowledge in marketing for the benefit of both the academia and business. Sports Medicine2016 is where the future of Sports Medicine and Fitness intersects. This event brings together the most of the eminent persons, researchers, scientists to explore there invaluable knowledge. Sports Medicine2016 is where Sports marketers go to gain perspective on the latest Sports technologies, emerging start-ups, and opportunities that will drive the future of the Sports Medicine and Fitness. We bring together business, creative, and technology leaders from the Sports Medicine market and Sports Medicine industry for the most current and relevant.

Why Dubai?

Dubai has emerged as a global city and business hub of the Persian Gulf region. It is also a major transport hub for passengers and cargo. It is a world’s fastest growing economies, Dubai’s gross domestic product is projected at USD 107.1 billion, with a growth rate of 6.1% in 2014. It is estimated that Dubai produces 50,000 to 70,000 barrels (7,900 to 11,100 m3) of oil a day and substantial quantities of gas from offshore fields.

Architecture: Dubai has a rich collection of buildings and structures of various architectural styles. Many modern interpretations of Islamic architecture can be found here. Burj Khalifa (The 828 meters tallest building in the world and a skyscraper in Dubai, UAE. It is a world-class destination and the magnificent place at Downtown Dubai), Burj Al Arab (The Burj Al Arab (Arabic: , Tower of the Arabs) is a 7 star luxury hotel. Although the hotel is frequently described as “the world’s only seven-Star hotel) Dubai, Miracle Garden (On Valentine’s Day 2013, the Dubai Miracle Garden, a 72,000-square meter flower garden, opened in Dubai land. It is currently the world’s largest flower garden. It has 45 million flowers with re-use of waste water through drip irrigation)

Food: Arabic food is very popular and is available everywhere in the city, from the small shawarma diners in Deira and Al Karama to the restaurants in Dubai’s hotels. Fast food, South Asian, and Chinese cuisines are also very popular and are widely available. Dubai is known for its nightlife. Clubs and bars are found mostly in hotels due to the liquor laws. The New York Times described Dubai as “the kind of city where you might run into Michael Jordan at the Buddha Bar or stumble across Naomi Campbell celebrating her birthday with a multiday bash”

Sports: Football and cricket are the most popular sports in Dubai which attract sports stars from around the world. The Dubai World Cup, a thoroughbred horse race, is held annually at the Meydan Racecourse. Dubai also hosts the traditional rugby union tournament Dubai Sevens, part of the Sevens World Series. In 2009, Dubai hosted the 2009 Rugby World Cup Sevens.

Conference Highlights:

Sports and Health

Sports Education and Sports Training

Exercise Physiology and Role of Hormones in Sport and Fitness

Injuries and Orthopedic Surgeries in Sports and Fitness

Sports Nutrition and Sports Medicine

Physical Therapies for Multiple Diseases

Technologies Assisting Sport and Exercise Facilitation

Computer Science Involved In Sports Science

Motor Skill Acquisition and Sports Psychology

Multidisciplinary Contributions To Sports Science

Natural or Herbal Medicine for Sports

Special Focus for 2016: Sport and Development

Why to attend???

Sports Medicine is one of the most important topic, With members from around the world focused on learning about Sports, physical health and other sports related activities, this is your single best opportunity to reach the largest assemblage of participants from the Sports and health community. Conduct demonstrations, distribute information, meet with current and potential Researchers, Scientists, Business Personals, and Industrialis , make a splash with an invaluable knowledge and receive name recognition at this 3-day event. World-renowned speakers, the most recent techniques, tactics, and the newest updates in Sports Medicine and Fitness fields are hallmarks of this conference.

A Unique Opportunity for Advertisers and Sponsors at this International event:

Major Sports Medicine Universities, colleges/Institutions around the world

George Washington University

University of Michigan (UM)

University of Pittsburgh

University of the Rockies

Iowa State University

The University of Alabama

American InterContinental University

Major Sports Medicine Universities, colleges/Institutions in UAE

American University of Sharjah

United Arab Emirates University

Northumbria University

University of Sharjah

Paris-Sorbonne University Abu Dhabi

Major Sports Medicine Universities, colleges/Institutions in Dubai

ETA College

New York University in Abu Dhabi

Dubai British School

Statistical Analysis of Sports Medicine Universities:

Major Sports Medicine Associations around the Globe

International Society of Arthroscopy, Knee Surgery and Orthopaedic Sports Medicine.

The International Sports Sciences Association (ISSA) USA

International Council of Sport Science and Physical Education (ICSSPE) Germany

Indian Association of Sports Medicine (IASM)

American Academy of Podiatric Sports Medicine

American Medical Societies for Sports medicine and The British Association of Sports and Medicine

Canadian Academy of Sport Medicine

World Institute of Sports Sciences (WISS), Florida

The South African Sports Medicine Association

California Association for Health, Physical Education, Recreation and Dance (CAHPERD)

The Association for the Advancement for Applied Sport Psychology

The European Federation of Sport Psychology

British Association of Sport and Exercise Science (BASES)

Brazilian College of Sport Science (CBCE)

Sport and Exercise Science New Zealand (SESNZ)

Sports Medicine Australia (SMA)

Japanese Association of University Physical Education and Sports

Centre for Orthopaedic Surgery, Switzerland

Major Sports Medicine Associations and Societies in UAE

Abu Dhabi Knee & Sports Medicine Centre

UAE Football Association

Dubai Sports Council

General Authority of youth and sports welfare

Emirates Motor Sports Federation

American Orthopaedic Society for Sports Medicine

Emirates Society of Emergency Medicine

Major Sports Medicine Associations and Societies in Dubai

International Knee and joint Center

UAE Health & Sports Medicine Centre

Physiotherapy and Rehabilitation Centre

The California Chiropractic and Sports Medicine Center

The City Hospital Dubai Healthcare City

Statistical Analysis of Sports Medicine Associations and societies:

Major hospitals and clinic of Sports Medicine around the world

Mayo Clinic Sports Medicine Center

The Sports Medicine Clinic, USA

Sports Medicine Clinic, Singapore

Seattle Childrens Hospital

UCSF Medical Center, USA

Foot & Leg Pain Clinics, Australia

The Stanford Health Care, USA

Fairview Sports and Orthopedic Care

Petts Wood Osteopathic Clinic, UK

Spectrum Physio Centre, India

UniSports Sports Medicine, New Zealand

Premiere Chiropractic & Sports Medicine, USA

Major hospitals and clinic of Sports Medicine in UAE

Sports Injury Clinic Abu Dhabi

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