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The starch in wheat has very high GI, and can lead to diabetes type 2, heart disease and all the other consequences of metabolic syndrome. I wrote this correction just to set the record straight. In other projects Wikimedia Commons. See image below for details. Tombland The Shardlake series.
Atkins has evolved from the s to now allowing a lot more fiber into the diet. It does have some grains of truth just like most incomplete science from the eighties. The problem ended up being trans fats and saturated fat not just fat. We all bought into the high carb low fat concept. Well now the science of healthy fats is well documented and insulin resistance science is being understood. High protein can also raise insulin so you are correct about too much protein not to mention all meat is not the same.
Processed meat and meat with GMOs hormones added and steroids are all a problem. Must be grass fed organic meet omega 3 rather than 6. But you probably need to re examine your information based on current science. Carbs are cancer fuel. Need a healthy balance but that balance should be much lower in carbs than has been pushed for the last 30 years.
I have been on a keto diet for the last couple months. I did have a gout attack at first but I attribute that to losing weight so rapidly. After that I have been absolutely fine.
My BP is about as normal as it gets. I have been enjoying my high fat and protein diet. I feel better than I have in years. Doctors have agreed for a long time on low carb for people with diabetes and people with epilepsy, and now most nutritional scientists and may doctors are starting to align in that the shift to the low fat, high carb is what has created the obesity epidemic we have today. The food pyramid is part of the problem, and even the government is backing away from that. I met Dr Atkins at his office for a full check up at his office within 2 months prior to his death.
He was NOT obese. He died after slipping on ice following a bad ice storm which I recall. I would agree to disagree. There is plenty of evidence that it is a unhealthy diet and dangerous. I know the Atkins fans are fanatical about this diet though. Spiro, your write up was crap.
I know a former Mr Universe and have a cell ph number of a former Mr Olympia in my contacts list. As well as the professional coroner if you think about it that verified Mr Atkins cause of death.
On several points you run like a mad man with speculation and hearsay as if its fact. Feelings do NOT make facts. Even if you sprinkle them with a few pieces of truth. Max, I know you pro Atkins diet pro Paleo diet, protein, protein, protein, gain muscle, gain muscle types hate what I have to say. The truth is you are all hurting yourselves inside. Outside may look good, but your kidneys are taking a beating by giving it all that protein to process and break down. I admit this is a controversial topic but if I am not so credible why is Tom Brady follow a plant based diet?
He is 39 years old and will play well into his mid-forties. He is still at his peak while everybody else is in decline at that age. There are many more athletes who are changing their diet to a plant based one, I predict in a few years that all this Paleo and protein diets will become obsolete and wither away.
That is my 2 cents. The content in your posts is further proof of your lack of qualification. More importantly, you are dispensing information to people with a potentially serious medical condition, based on sources like Wikipedia. It is apparent that you are unqualified to interpret scientific study results. Much less disseminate said info to an unsuspecting public.
I read your article on drinking. However, if out with friends or at an event,other than beer, is there any other type of adult drink that is less harmful on gout sufferers? Alcohol is alcohol, avoid it if you can. Actually the Atkins diet is a high fat, moderate protein, and low sugar and starch diet. The aim of the diet is to reduce insulin, and both protein and carbohydrate stimulate insulin production. Leafy greens, psyllium and Chia provide fibre without digestible carbohydrate.
Most arguments against Atkins are straw man arguments, they falsely claim Atkins is high protein, low fibre, then criticize that obviously bad diet. Grains like wheat should be avoided by many people, as wheat gliadin can cause leaky gut syndrome, which, in genetically susceptible people, can lead to autoimmune diseases like: Celiac disease, diabetes type 1, thyroiditis, gluten ataxia, psoriasis, vitiligo, autoimmune hepatitis, dermatitis herpetiformis, primary sclerosing cholangitis etc.
The starch in wheat has very high GI, and can lead to diabetes type 2, heart disease and all the other consequences of metabolic syndrome.
People who suffer from gout should avoid fructose. Following a properly formulated low sugar and starch diet will usually help avoid gout. His weight at the time of the fall was , at the high end of normal range, not obese. The underlying cause of death was blunt force trauma to the head resulting in an epidural hematoma, which caused coma of 9 days from the time of the fall until death.
The immediate cause of death was complications of surgery to relieve the hematoma. Fluid retention caused severe bloating and weight gain of 63 pounds. That is why he appeared grossly obese at death. The wife objected to autopsy, so the Medical Examiner only examined the body externally, noting appearance and weight, as well as the history of heart attack some years earlier. Therein lies the misunderstanding.
Having said fhat, I do not favor his diet, as high protein consumption can be deadly for someone like myself with asthma and kidney problems as well as arthritis and gout. I wrote this correction just to set the record straight. I hear you Bruce, but the evidence suggests and if you look at the Wikipedia entry, it states: This information is so out of date.
As a gout sufferer I have been through the problems and tried many diets. Latest research has found that gout is strongly associated with diabetes and insulin resistance and that fructose i. Higher intake of Vitamin C is believed to combat high uric acid levels worked for me. For us gout sufferers ketosis and extreme low carb diets should be avoided. So enjoy average amount od red meats and seafood as they have been exonerated — I eat them all the time and have not had a gout attack since changing to the above recommendations.
What you are saying is totally off the mark! I know the carnivore eaters hate me but there is no real research showing that eating meat in such abundance is good for your health in any way.
Also outside of science, common sense should also tell you that! Come one, seafood being healthy? A diet high in animal protein is what is causing most of the diseases we have to deal with today. Read research papers not only from North America but from Asian studies as well.
I was on the Atkins diet for years and never lost an ounce. So none of it made sense to me. Back then, I was having more trouble with sugar and yeast hypoglycemia and candidiasis from antibiotics.
Gluten and celiac sprue was another one. Anyway, gout sufferers have the worst diet restrictions because almost nothing is safe, including our own bodies. Spinach, broccoli, asparagus, beans, peas, eggs, tofu, tomatoes and cauliflower have to be watched too. Gout meds all stink too. Thus far, talking to doctors has proven useless. They know less about gout than we do.
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Experiments on Battling Gout. Is the Atkins diet good for gout patients? The primary effect of leptins is in the hypothalamus , a part of the central nervous system. Leptin receptors are expressed not only in the hypothalamus but also in other brain regions, particularly in the hippocampus. Thus some leptin receptors in the brain are classified as central hypothalamic and some as peripheral non-hypothalamic.
Generally, leptin is thought to enter the brain at the choroid plexus , where the intense expression of a form of leptin receptor molecule could act as a transport mechanism.
Increased levels of melatonin causes a downregulation of leptin,  however, melatonin also appears to increase leptin levels in the presence of insulin , therefore causing a decrease in appetite during sleeping. Mice with type 1 diabetes treated with leptin or leptin plus insulin, compared to insulin alone had better metabolic profiles: Leptin acts on receptors in the lateral hypothalamus to inhibit hunger and the medial hypothalamus to stimulate satiety.
Thus, a lesion in the lateral hypothalamus causes anorexia due to a lack of hunger signals and a lesion in the medial hypothalamus causes excessive hunger due to a lack of satiety signals. The absence of leptin or its receptor leads to uncontrolled hunger and resulting obesity. Fasting or following a very-low-calorie diet lowers leptin levels.
Leptin binds to neuropeptide Y NPY neurons in the arcuate nucleus in such a way as to decrease the activity of these neurons. Leptin signals to the hypothalamus which produces a feeling of satiety. Moreover, leptin signals may make it easier for people to resist the temptation of foods high in calories.
The NPY neurons are a key element in the regulation of hunger; small doses of NPY injected into the brains of experimental animals stimulates feeding, while selective destruction of the NPY neurons in mice causes them to become anorexic. Once leptin has bound to the Ob-Rb receptor, it activates the stat3, which is phosphorylated and travels to the nucleus to effect changes in gene expression, one of the main effects being the down-regulation of the expression of endocannabinoids , responsible for increasing hunger.
It modulates the immune response to atherosclerosis, of which obesity is a predisposing factor. Exogenous leptin can promote angiogenesis by increasing vascular endothelial growth factor levels. Hyperleptinemia produced by infusion or adenoviral gene transfer decreases blood pressure in rats. Leptin microinjections into the nucleus of the solitary tract NTS have been shown to elicit sympathoexcitatory responses, and potentiate the cardiovascular responses to activation of the chemoreflex.
In fetal lung, leptin is induced in the alveolar interstitial fibroblasts "lipofibroblasts" by the action of PTHrP secreted by formative alveolar epithelium endoderm under moderate stretch.
The leptin from the mesenchyme, in turn, acts back on the epithelium at the leptin receptor carried in the alveolar type II pneumocytes and induces surfactant expression, which is one of the main functions of these type II pneumocytes. In mice, and to a lesser extent in humans, leptin is required for male and female fertility. Ovulatory cycles in females are linked to energy balance positive or negative depending on whether a female is losing or gaining weight and energy flux how much energy is consumed and expended much more than energy status fat levels.
When energy balance is highly negative meaning the woman is starving or energy flux is very high meaning the woman is exercising at extreme levels, but still consuming enough calories , the ovarian cycle stops and females stop menstruating. Only if a female has an extremely low body fat percentage does energy status affect menstruation. Leptin levels outside an ideal range may have a negative effect on egg quality and outcome during in vitro fertilization.
The placenta produces leptin. Leptin is also expressed in fetal membranes and the uterine tissue. Uterine contractions are inhibited by leptin. Immunoreactive leptin has been found in human breast milk; and leptin from mother's milk has been found in the blood of suckling infant animals.
Leptin along with kisspeptin controls the onset of puberty. Leptin's ability to regulate bone mass was first recognized in Leptin decreases cancellous bone , but increases cortical bone. This "cortical-cancellous dichotomy" may represent a mechanism for enlarging bone size, and thus bone resistance, to cope with increased body weight.
Bone metabolism can be regulated by central sympathetic outflow, since sympathetic pathways innervate bone tissue. Factors that acutely affect leptin levels are also factors that influence other markers of inflammation, e.
While it is well-established that leptin is involved in the regulation of the inflammatory response,    it has been further theorized that leptin's role as an inflammatory marker is to respond specifically to adipose-derived inflammatory cytokines. In terms of both structure and function, leptin resembles IL-6 and is a member of the cytokine superfamily. Similar to what is observed in chronic inflammation, chronically elevated leptin levels are associated with obesity, overeating, and inflammation-related diseases, including hypertension , metabolic syndrome , and cardiovascular disease.
While leptin is associated with body fat mass, however, the size of individual fat cells, and the act of overeating, it is interesting that it is not affected by exercise for comparison, IL-6 is released in response to muscular contractions.
Thus, it is speculated that leptin responds specifically to adipose-derived inflammation. Taken as such, increases in leptin levels in response to caloric intake function as an acute pro-inflammatory response mechanism to prevent excessive cellular stress induced by overeating. When high caloric intake overtaxes the ability of fat cells to grow larger or increase in number in step with caloric intake, the ensuing stress response leads to inflammation at the cellular level and ectopic fat storage, i.
The insulin increase in response to the caloric load provokes a dose-dependent rise in leptin, an effect potentiated by high cortisol levels. This response may then protect against the harmful process of ectopic fat storage, which perhaps explains the connection between chronically elevated leptin levels and ectopic fat storage in obese individuals.
Although leptin reduces appetite as a circulating signal, obese individuals generally exhibit a higher circulating concentration of leptin than normal weight individuals due to their higher percentage body fat. A number of explanations have been proposed to explain this.
An important contributor to leptin resistance is changes to leptin receptor signalling, particularly in the arcuate nucleus , however, deficiency of, or major changes to, the leptin receptor itself are not thought to be a major cause. Other explanations suggested include changes to the way leptin crosses the blood brain barrier BBB or alterations occurring during development.
Studies on leptin cerebrospinal fluid CSF levels provide evidence for the reduction in leptin crossing the BBB and reaching obesity-relevant targets, such as the hypothalamus, in obese people. Since the amount and quality of leptin receptors in the hypothalamus appears to be normal in the majority of obese humans as judged from leptin-mRNA studies ,  it is likely that the leptin resistance in these individuals is due to a post leptin-receptor deficit, similar to the post-insulin receptor defect seen in type 2 diabetes.
When leptin binds with the leptin receptor, it activates a number of pathways. Mice with a mutation in the leptin receptor gene that prevents the activation of STAT3 are obese and exhibit hyperphagia. The PI3K pathway may also be involved in leptin resistance, as has been demonstrated in mice by artificial blocking of PI3K signalling.
The PI3K pathway also is activated by the insulin receptor and is therefore an important area where leptin and insulin act together as part of energy homeostasis.
The consumption of a high fructose diet from birth has been associated with a reduction in leptin levels and reduced expression of leptin receptor mRNA in rats. Long-term consumption of fructose in rats has been shown to increase levels of triglycerides and trigger leptin and insulin resistance,   however, another study found that leptin resistance only developed in the presence of both high fructose and high fat levels in the diet.
A third study found that high fructose levels reversed leptin resistance in rats given a high fat diet. The contradictory results mean that it is uncertain whether leptin resistance is caused by high levels of carbohydrates or fats, or if an increase of both, is needed. Leptin is known to interact with amylin , a hormone involved in gastric emptying and creating a feeling of fullness.
When both leptin and amylin were given to obese, leptin-resistant rats, sustained weight loss was seen. Due to its apparent ability to reverse leptin resistance, amylin has been suggested as possible therapy for obesity. It has been suggested that the main role of leptin is to act as a starvation signal when levels are low, to help maintain fat stores for survival during times of starvation, rather than a satiety signal to prevent overeating.
Leptin levels signal when an animal has enough stored energy to spend it in pursuits besides acquiring food. Dieters who lose weight, particularly those with an overabundance of fat cells, experience a drop in levels of circulating leptin. This drop causes reversible decreases in thyroid activity, sympathetic tone, and energy expenditure in skeletal muscle, and increases in muscle efficiency and parasympathetic tone.
A decline in levels of circulating leptin also changes brain activity in areas involved in the regulatory, emotional, and cognitive control of appetite that are reversed by administration of leptin. Osteoarthritis and obesity are closely linked. Obesity is one of the most important preventable factors for the development of osteoarthritis. Originally, the relationship between osteoarthritis and obesity was considered to be exclusively biomechanically based, according to which the excess weight caused the joint to become worn down more quickly.
However, today we recognise that there is also a metabolic component which explains why obesity is a risk factor for osteoarthritis, not only for weight-bearing joints for example, the knees , but also for joints that do not bear weight for example, the hands. Thus, the deregulated production of adipokines and inflammatory mediators, hyperlipidaemia, and the increase of systemic oxidative stress are conditions frequently associated with obesity which can favour joint degeneration.
Furthermore, many regulation factors have been implicated in the development, maintenance and function, both of adipose tissues, as well as of the cartilage and other joint tissues. Alterations in these factors can be the additional link between obesity and osteoarthritis. Adipocytes interact with other cells through producing and secreting a variety of signalling molecules, including the cell signalling proteins known as adipokines.
Certain adipokines can be considered as hormones, as they regulate the functions of organs at a distance, and several of them have been specifically involved in the physiopathology of joint diseases. In particular, there is one, leptin, which has been the focus of attention for research in recent years.
The circulating leptin levels are positively correlated with the Body Mass Index BMI , more specifically with fatty mass, and obese individuals have higher leptin levels in their blood circulation, compared with non-obese individuals. In addition to the function of regulating energy homeostasis, leptin carries out a role in other physiological functions such as neuroendocrine communication, reproduction, angiogenesis and bone formation.
More recently, leptin has been recognised as a cytokine factor as well as with pleiotropic actions also in the immune response and inflammation. Leptin has thus emerged as a candidate to link obesity and osteoarthritis and serves as an apparent objective as a nutritional treatment for osteoarthritis. As in the plasma, the leptin levels in the synovial fluid are positively correlated with BMI. Leptin has been shown to be produced by chondrocytes, as well as by other tissues in the joints, including the synovial tissue, osteophytes, the meniscus and bone.
The risk of suffering osteoarthritis can be decreased with weight loss. This reduction of risk is related in part with the decrease of the load on the joint, but also in the decrease of fatty mass, the central adipose tissue and the low-level inflammation associated with obesity and systemic factors.
This growing evidence points to leptin as a cartilage degradation factor in the pathogenesis of osteoarthritis, and as a potential biomarker in the progression of the disease, which suggests that leptin, as well as regulation and signalling mechanisms, can be a new and promising target in the treatment of osteoarthritis, especially in obese patients. Obese individuals are predisposed to developing osteoarthritis, not only due to the excess mechanical load, but also due to the excess expression of soluble factors, that is, leptin and pro-inflammatory cytokines, which contribute to joint inflammation and cartilage destruction.
As such, obese individuals are in an altered state, due to a metabolic insufficiency, which requires specific nutritional treatment capable of normalising the leptin production and reducing the systematic low-level inflammation, in order to reduce the harmful impact of these systematic mediators on the joint health.
There are nutritional supplements and pharmacological agents capable of directing these factors and improving both conditions. Leptin was approved in the United States in for use in congenital leptin deficiency and generalized lipodystrophy. An analog of human leptin metreleptin trade name Myalept was first approved in Japan in , and in the United States in February In the US it is indicated as a treatment for complications of leptin deficiency, and for the diabetes and hypertriglyceridemia associated with congenital or acquired generalized lipodystrophy.
From Wikipedia, the free encyclopedia. Not to be confused with Lectin or Lecithin. Structure of the obese protein leptin-E Leptin plays a critical role in the adaptive response to starvation.
Leptin receptor and Energy expenditure. Bearing in mind that other hormones such as ghrelin operate in a faster-time scale, it would be misleading to define it as "the satiety hormone". Nat Clin Pract Endocrinol Metab.