Societal vs Genetic

 There is an ongoing controversy that various populations have certain health related issues due to their societal conditions versus a genetic profile. Consider the issue of obesity. Obesity all too often leads to Type 2 Diabetes, T2D, and related health impacts, Thus the sequence of obesity then T2D then cardiac and renal issues is common. It is well known that this is common in Native Americans. Native Americans have a strong genetic trait to survive and prosper on limited caloric intake. Like many other stressed ethnicity this factor get eliminated in an advanced society such as the US and obesity occur due to the proliferation of high caloric food intake. The sequellae are then inevitable,

In a recent paper by Sun et al they note:

Preferential fat accumulation in visceral vs. subcutaneous depots makes obese individuals more prone to metabolic complications. Body fat distribution (FD) is regulated by genetics. FD patterns vary across ethnic groups independent of obesity. Asians have more and Africans have less visceral fat compared with Europeans. Consequently, Asians tend to be more susceptible to type 2 diabetes even with lower BMIs when compared with Europeans. To date, genome-wide association studies (GWAS) have identified more than 460 loci related to FD traits. However, the majority of these data were generated in European populations. In this review, we aimed to summarize recent advances in FD genetics with a focus on comparisons between European and non-European populations (Asians and Africans). We therefore not only compared FD-related susceptibility loci identified in three ethnicities but also discussed whether known genetic variants might explain the FD pattern heterogeneity across different ancestries. Moreover, we describe several novel candidate genes potentially regulating FD, including NID2, HECTD4 and GNAS, identified in studies with Asian populations. It is of note that in agreement with current knowledge, most of the proposed FD candidate genes found in Asians belong to the group of developmental genes 

Thus one may observe that the genetic predisposition is dominant. This genetic predisposition all too often is the controlling factor and not societal constraints. Also generally it demands education of this fact and remediation to assure that the negative effects are minimized. No patient or person is the same but some generalizations may be helpful.

Obesity and Error; A Tale of Political Correctness gone Astray

In a long piece in what seems in my opinion to have become the world's paper of scientific record, The Huffington Post, a major contribution to humanity brought to you by Verizon, is a lengthy article on obesity, and apparently why all of science and medicine are in error[1]. Now the current view is that for the most part, significant endocrine pathologies excluded, obesity is a simple input less output issue. Eat more, burn less, gain weight. Second, obesity triggers a plethora of cell pathway damages and assaults, including but not limited to an explosion of reactive oxygen species. We have written about this extensively[2].

One simple and continuously provable result is in Type 2 diabetes. Drop the BMI below say 23 and the HbA1c drops back to a normal range below 5.5. The net result is the sequella common in that disease also often disappear. That is just one provable example.

In the UK a recent report by Cancer Research UK notes[3]:

And if these trends in the number of cases caused by these risk factors continue, overweight and obesity could overtake smoking as the biggest preventable cause of cancer in women by 2043. While the gap between obesity and tobacco as causes of cancer in men is also expected to narrow in the next 20 years, there’s still a way to go before they cross over. And it’s too soon to estimate when this might happen. The crossover is likely to happen earlier in women for two reasons. First, more men smoke than women. And that means there are more smoking-related cancers in men. In 2015, 18% of cancer cases in men were caused by smoking, compared with just 12% in women. And while men are also more likely to be overweight or obese than women, obesity has a bigger effect on women in terms of cancer. Some of the most common types of cancer caused by obesity are breast and womb cancer, which predominantly affect women.

The writer in the above mentioned Huffington Post peer reviewed (?) scientific article goes at length to argue that obesity is not self-inflicted and that obese people are more often healthier than those of lesser girth. That would be just fine if and only if the clear and demonstrable costs of obesity were not borne primarily by those who themselves struggle to maintain a reasonable weight and avoid the multiplicity of sequella to high BMI. Frankly if health care costs were borne by each individual as they occur to that individual, and there is no secondary effect of their behavior on others, no externalities so to speak, then frankly anyone should be able to do anything. Unfortunately the same people demand Medicare for all, as such those costs would explode.

The same people who felt no compunction to shaming smokers, a truly valuable action considering the decline in death rates in males, seem now to think any form of negative connotations regarding an often self-inflicted condition which also all too often results in massive health care costs, borne by all, is not only socially unacceptable but tantamount to criminal. Furthermore, like so many of the "unacceptable" position it is also worthy of assault on those who demur.

We seem to entering a generation tsunami where what one says must be true no matter what and facts be damned. Even more so, anyone who dares to use science and facts, other than to reinforce the position of the week is anathema.

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[1] https://highline.huffingtonpost.com/articles/en/everything-you-know-about-obesity-is-wrong/

[2] https://www.researchgate.net/publication/265206539_Obesity_and_Type_2_Diabetes_Cause_and_Effect?_sg=dV5aHikCis5L_AYSHTRyuj_b-tWIxvaMa1jvpPEMWpPKO8anCOj4WS4T9Q26u9sism0fkWnpz01s3jTVOjPuRE5TDL4IqU_KsFuM-AIu.TlZzoo4W12VLPWh26RtmAlF8uXfC1cSrSw7dydyhHxvOLMRTn_ZvcZsU8Dwlg4t8SqXkvZ-jamlOnKAhrj7mpQ

[3] https://scienceblog.cancerresearchuk.org/2018/09/24/how-we-estimated-when-obesity-might-catch-smoking-as-the-top-cause-of-cancer/

An Externality of Obesity

Externalities, those economic factors which a student is introduced to and spends most of their undergraduate days trying to understand. So try this one on.

The Telegraph reports:

But according to new reports emerging from Santorini, this scenery is now coming at a high cost in animal cruelty, with the price being paid by the island's donkey population. The practice of selling donkey rides to visitors is attracting growing criticism from animal welfare groups, who argue that the creatures are being forced to carry excessive numbers of increasingly overweight tourists from the UK, the USA and Russia. Coming in for particular fire is the busy route up the cliffs of the west coast - from the harbour at sea level to the capital Fira, which sits some 400 metres (1,312 feet) above the water, on the ridge.

Yes, those obese tourists from the US, UK and now Russia. Where are the Germans may I ask?

My experience over the years has shown that American style foods and worse American style servings are the cause. They first infiltrated the UK. I saw this about twenty years ago. The Pret a Manger sandwich shops went from small French style servings to Manhattan style colossal sandwiches. Then the Brits added fries and beer! Tie that on at lunch and then try to do anything for the rest of the day.

The poor donkeys.

More Evidence

As we just noted, obesity can be a major driver for cancer. Moreover obesity, even just being over weight, can be the driver for Type 2 Diabetes. That in turn drives kidney, heart, and nerve/eye failure. Unlike smoking and lung cancer, where the patient generally dies in six to nine months, Type 2 Diabetes is chronic costing billions.

In the UK, the NHS hands out pills. The solution is quite simple. Lose weight, stop junk food. Better yet, tax obesity, file your tax return and get weighed. Imagine what that would do for some Presidents! But that is another tale.

In the US, according to the NY Times, we send them to a class. We seem to have classes for everything; Diversity, Harassment, Quality, Ethics, etc. The Trainers get billions and we are then left with sick fat folks spending billions on Big Pharma pills.

As the Times notes:

There are about 1.5 million Americans newly diagnosed with Type 2 diabetes each year, a disease typically associated with excess weight and a sedentary lifestyle. Diabetes self-management programs teach patients how to monitor their blood sugars, what to eat and the importance of exercise as strategies to delay or avoid the disease’s serious complications....Diabetes is among the costliest of medical conditions. The American Diabetes Association estimates that average medical expenditures for those with diabetes diagnoses are 2.3 times higher than those without...One of the most expensive — a 7½-hour diabetes self-management group course that included two-hour individual sessions with a dietitian and a diabetes educator — cost $1,700 in Washington state....

You do not need a course. You need a physician to call it for what it is, not a disease, but the patient's problem, they eat too much! Perhaps we should start weighing and taxing based on BMI.

Obesity and Cancer

We have recently examined the issues of inflammation and cancer as well as the microbiome and cancer. A long standing relationship is with obesity and cancer. Obesity increases inflammation as well as altering the microbiome. Science notes:

Obesity-associated inflammation (OAI) can dramatically alter tissue composition, thereby creating a fertile soil for cancer development; it is conceivable that these changes may lower mutational and epigenetic barriers to tumorigenesis. For instance, in breast and pancreas, OAI is associated with altered extracellular matrix composition that facilitates transformation of premalignant cells. In the colon, epigenetic alterations that occur in cancer are observed in normal epithelial cells in the context of obesity, thus lowering the mutational threshold that is required for malignant transformation. These studies suggest that OAI “primes” both the tissue microenvironment and premalignant epithelial cells to facilitate oncogenic transformation. Indeed, obesity is often associated with specific molecular subtypes of cancer, which may reflect a selective pressure exerted by the obese microenvironment resulting in the altered fitness of specific oncogenic mutations. Accordingly, tumors that evolve within an obese microenvironment may exhibit “obesity addiction” whereby they are driven by a dependency on hypernutrition and inflammatory cytokines.

It is interesting that fifty years ago we were all worried about the lack of food for humans. Now we have a massive explosion of obesity. Food seems no longer to be a global issue. But the sequellae from excess food may very well be more dire.

I Don't Think So

The NY Times discusses the weight gain/loss issue and blames the brain rather than will power. They state:

The root of the problem is not willpower but neuroscience. Metabolic suppression is one of several powerful tools that the brain uses to keep the body within a certain weight range, called the set point. The range, which varies from person to person, is determined by genes and life experience. When dieters’ weight drops below it, they not only burn fewer calories but also produce more hunger-inducing hormones and find eating more rewarding.

No the root problem is that 3500 Kcal equals one pound. And if you only burn 1200 Kcal per day you have a problem if you consume 2400 Kcal per day, you gain 1 pound every 3 days! Now the problem is burn rate. Genetic control has allowed certain peoples to live on fewer calories. Native Americans in certain areas were living off of very few calories and when introduced to a European diet one saw massive levels of obesity and Type 2 Diabetes. When they had fewer calories they did well and survived, it was the diet change that did it.

The problem in my opinion is what we allow ourselves to consume as food. Often also it is the spouse or family that is non-supportive and almost antagonistic to the dieter. The environment during the weight loss period is focused but then after it returns to an excess caloric one where all too often family members reinforce the eating misalignment.

Thus it may very well be will power, but the will power of the family and friends to change.

Obesity and Genes; Redux

There seems to be a continuing search for the genes which "cause" obesity. To reiterate, independent of any gene;

Input - Output = Net Accumulation

Thus eat too much means you get fat. Of course the problem with the above is; how does one measure input and output. The classic manner is in food and Kcal. Thus:

3500 Kcal = 1 pound

That is for every 3500 Kcal one consumes above a Basal Metabolism burn rate one gains a pound.

However not all food is equal and not all people burn calories at the same rate. Thus perhaps there is a genetic factor on burn rates. That does not negate the above argument.

Into this fray is a new article in NEJM. They state:

Our results point to a pathway for adipocyte thermogenesis regulation involving ARID5B, rs1421085, IRX3, and IRX5, which, when manipulated, had pronounced pro-obesity and anti-obesity effects.

 This is 3 genes and a single SNV. But we must always ask; what is the cause? Again it appears that with these genes fat cells burn at a lower rate. Thus if a normal person, whatever that means, can deal with 1800 Kcal per day and not gain weight then a gene encumbered person may only burn 1200 Kcal per day and eating the same amount will thus gain weight. So eat less! The cause of obesity is consumption. If one has a lower set point then eat less.

Now in the MIT write up of this article the authors state:

But there may now be a new approach to prevent and even cure obesity, thanks to a study led by researchers at MIT and Harvard Medical School and published today in the New England Journal of Medicine. By analyzing the cellular circuitry underlying the strongest genetic association with obesity, the researchers have unveiled a new pathway that controls human metabolism by prompting our adipocytes, or fat cells, to store fat or burn it away. “Obesity has traditionally been seen as the result of an imbalance between the amount of food we eat and how much we exercise, but this view ignores the contribution of genetics to each individual’s metabolism,” says senior author Manolis Kellis, a professor of computer science and a member of MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL) and of the Broad Institute.

 Well frankly the CSAIL reference is wrong. It does not relate to exercise bu cell burn rates. We always knew that. We further know that some people's cells burn at different rates and that obese people burn at a lower rate. The classic case is the Southwest Indian Tribes who most likely after generations have adapted to low caloric input due to the nature of their environment and thus have a lower conserving burn rate. We see this in many immigrants from countries where food was no readily available. The Irish and many Hispanics have a similar characteristic. (Also some early epigenetic studies demonstrated inheritable traits from WW II starvation in the Low Countries).They can maintain lower weight by not eating our high calorie foods. Don't blame the genes, in fact the genes have adapted to the harsh limited food environment which may be beneficial.

The NEJM article concludes:

Last, we found that direct manipulation of the ARID5B–rs1421085–IRX3/IRX5 regulatory axis in primary cell cultures of adipocytes from patients reversed the signatures of obesity. This indicates that in addition to changes in physical activity and nutrition, manipulation of mitochondrial thermogenesis offers a potential third pathway for shifting between energy storage and expenditure in a brain-independent and tissue-autonomous way in humans. In summary, our work elucidates a mechanistic basis for the strongest genetic association with obesity. Our results indicate that the SNV rs1421085 underlies the genetic association between the FTO locus and obesity. The SNV disrupts an evolutionarily conserved motif for the ARID5B repressor, which leads to loss of binding, derepression of a potent preadipocyte superenhancer, and activation of downstream targets IRX3 and IRX5 during early differentiation of mesenchymal progenitors into adipocyte subtypes. This results in a cell-autonomous shift from white adipocyte browning to lipid-storage gene expression programs and to repression of basal mitochondrial respiration, a decrease in thermogenesis in response to stimulus, and an increase in adipocyte size. Manipulation of the uncovered pathway, including knockdown or overexpression of the upstream regulator ARID5B, genome editing of the predicted causal variant rs1421085, and knockdown or overexpression of target genes IRX3 and IRX5, had a significant effect on obesity phenotypes.

Now the last things we need is a new medication to control genetic pathways when the answer is just lower food consumption. That is free!

As an aside I found that the paper relied on murine samples. In addition they state:

To translate the results of genomewide association studies into mechanistic insights, we combined public resources (epigenomic annotations, chromosome conformation, and regulatory motif conservation), targeted experiments for risk and nonrisk haplotypes (enhancer tiling, gene expression, and cellular profiling), and directed perturbations in human primary cells and mouse models (regulator–target knockdown and overexpression and CRISPR–Cas9 genome editing). 

 Let's just hope we don't do CRISPR Cas9 editing on humans for obesity! Just a concern.

Oh and by the way, there is a very effective tool already in use. It is called the Scale. Cheap, lots of them around, and it provides a set point feedback loop. You get on it once a day and if it gets higher you stop eating, if it gets too low, then see a Doc!

And yes, one last thing, the MIT Stata Center where CSAIL is located has a "food court" I used to frequent, albeit carefully. The food there is carb rich, and more than likely will be the cause of later obesity issues. So one must always examine their own sand box, and not blame the genes for everything!

Obesity: A Scale versus the Genes

There is a continual debate over the idea that:

Input-Output=Net Accumulation

This is always true, by definition.

However we should always examine what we mean by each term. Let us first examine Input.

Input= the net amount of kcal an individual obtains by the consumption of a certain type of food

Now that will depend on the food and the individual. Certain people have enzymes, products of genes, that convert the consumed more efficiently, and they also have epigenetic factors that enhance conversion of the consumed food into products that can be used or stored. Thus Input for one person consuming the same food as another is NOT the same. Genes play a part in how the physical raw input is processed in the individual to stored and used Input in the body. Thus the net Input, that which is used and/or stored, may vary in some statistical manner between humans.

For example certain southwest Indian tribes have genes that allow highly efficient absorption meaning that they can live on poor quality food but give rich foods they explode in weight and Type 2 Diabetes. Another example, epigenetic, is from Netherlands in WW II where in 1944 mothers were starved by Nazis and children born had epigenetic marks that allowed them to survive on low caloric intake by up-regulating certain genes. Thus genetic and epigenetic factors affect the conversion of Input and the net result can vary. The epigenetic factors can be passed down to children and in some cases to grandchildren. Thus environment via epigenetic changes can affect the genetic makeup.

Having said this, one can develop a distribution of net Input as a function of Gross Input, namely consumed food, and see that across a large population there is, one can assume, a Gaussian like distribution. Some people, most if you will, have a conversion rate of say 1, others may have a larger or smaller conversion rate. It does not appear that a great deal has been done examining this factor.

Output is basal metabolism rate and other factors whereby we burn calories. That also varies dramatically. You walk 5 miles and I walk 5 miles and we each urn a different amount. Again Output may vary from individual to individual. I may burn 100 kcal per mile walked and another may bur 75 or 125 kcal. Why the difference? Again it may be an amalgam of genetic or epigenetic. It may also be the way one walks. Therefore Output like Input has some form of distribution across large populations.

The problem thus is neither Input nor Output, it is Net Accumulation. Thus for zero Net Accumulation we each must understand our balance. Now that also may change as we may face different challenges.

Humans have the ability to use their intellect to measure a set point, namely a scale and to measure their weight. Secondly humans have the will power and intellectual capability to retain that set point.

Other animals spend all day hunting for feed and consuming generally low calorie food, and somehow maintain a balance. Rarely do we see a fat squirrel

The conclusions are:

1. Environment does affect what we see as net Input and net Output and thus net Accumulation

2. Genetics and Epigenetics affect what each individual does in terms of conversions

3. However as humans we have the ability/intelligence to measure the set point and the will to maintain it.

4. One size fits all does not work. Each human is different in how they convert Gross Input to Net Input and Gross Output to Net Output. Thus the only true measure is the scale, namely weighing oneself and balancing Input and Output to keep the scale at the required set point.

Thus when writes in the NY Times and other journals of note speak of diet and weight control we hear them state[1]:

FOR most of the last century, our understanding of the cause of obesity has been based on immutable physical law. Specifically, it’s the first law of thermodynamics, which dictates that energy can neither be created nor destroyed. When it comes to body weight, this means that calorie intake minus calorie expenditure equals calories stored. Surrounded by tempting foods, we overeat, consuming more calories than we can burn off, and the excess is deposited as fat. The simple solution is to exert willpower and eat less. The problem is that this advice doesn’t work, at least not for most people over the long term. In other words, your New Year’s resolution to lose weight probably won’t last through the spring, let alone affect how you look in a swimsuit in July.

All too often they oversimplify all factors. The basic law holds, it is a definition, a tautology. The problem is the conversion rates from Gross to Net, a factor that the authors above seem to struggle with but in apparent ignorance. Basically they argue about some set point theory. Namely humans eat until the set point and then stop. Eat too much, get fat, the set point increases and the system is unstable. Fat Squirrels! However this totally ignores the scale. If the goal is a BMI of 24.0-25.0 worst case, then just use the scale, reduce food intake by the use of the will until the scale falls back to the right range, and forget these putative set points, namely blaming some other factor. Take responsibility.

The authors continue:

If this hypothesis turns out to be correct, it will have immediate implications for public health. It would mean that the decades-long focus on calorie restriction was destined to fail for most people. Information about calorie content would remain relevant, not as a strategy for weight loss, but rather to help people avoid eating too much highly processed food loaded with rapidly digesting carbohydrates. But obesity treatment would more appropriately focus on diet quality rather than calorie quantity.

Obesity treatment is a non-issue by using a scale. Yes indeed, forget the calories, measure the pounds. Scales are cheap!

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[1] http://www.nytimes.com/2014/05/18/opinion/sunday/always-hungry-heres-why.html?partner=rss&emc=rss

Input Less Output Equals Net Accumulation

A law of nature, if you burn 1800 Kcal per day and consume 2100 Kcal per day, then the excess of 300 Kcal over about 12 days will add one pound. Now today in the NY Times we have another excuse for obesity, antibiotics.

The author writes:

And yet, scientists still could not explain the mystery of antibiotics and weight gain. Nor did they try, really. According to Luis Caetano M. Antunes, a public health researcher at the Oswaldo Cruz Foundation in Brazil, the attitude was, “Who cares how it’s working?” Over the next few decades, while farms kept buying up antibiotics, the medical world largely lost interest in their fattening effects, and moved on. In the last decade, however, scrutiny of antibiotics has increased. Overuse of the drugs has led to the rise of antibiotic-resistant strains of bacteria — salmonella in factory farms and staph infections in hospitals. Researchers have also begun to suspect that it may shed light on the obesity epidemic.

 Now it is not only genes, advertising, it is also antibiotics. It may just as likely be global warming, climate change, or whatever the latest fad is. What it is, simply, is eating too many calories and expending too few. That law of nature has not changed. Perhaps the calories per pound of pork has increased, then eat less pork. 

All one has to do is go into any American restaurant. Large plates, immense portions of high calorie food and great numbers of obese people consuming the plates, one after another. Any one of the many chain restaurants serve massive platters of excess calories and the patrons consume the food with glee. There is no price, yet, for many of them, and their obesity. Yet as it continues to grow the costs will explode. 

There is no benefit to "discovering" new reasons why these people are fat. They eat too much. The whole business of blaming some exogenous factors when the fault lies within is a major failing of our society. For every 0.1 that a person is over a BMI of 25.0, there should be a tax of say $500. That ought to stem some of the tide. Sort of a new idea on income redistribution. Think about it.

Is There a Genetics of Human Obesity?

There seems to be a persistent search for the genetic basis of human obesity. Again the basic fact of  life is that 3500 kcal equal one pound of body weight. So if you burn 2000 kcal per day and consume 2350 per day you gain one pound in ten days. That is a simple law. Genes or no genes.

Now in a recent NYAS paper the authors search for the elusive cause, neglecting the apparent truth. They state:

Although a number of significant findings have been made, it appears that very little of the apparent heritability of body mass index has actually been explained to date. New approaches for data analyses and advances in technology will be required to uncover the elusive missing heritability, and to aid in  the identification of the key causative genetic underpinnings of obesity.

In the past two decades, family studies and animal models have helped us to identify many genetic
events associated with obesity. Subsequently, GWAS have driven the transition from primarily studying monogenic traits to ones of a more polygenic nature. GWAS have also revolutionized the genomics of obesity field, in that it offers an unbiased approach to uncover novel common genetic variants contributing to the pathogenesis of obesity.

Despite these great advances, the combined results of linkage, candidate gene, and GWAS approaches have explained very little of the variance in BMI, suggesting that there are still many  genetic findings to be made, most likely being rarer variants exhibiting small effects. In order to fully characterize this missing heritability, larger and larger sample sizes are going to be required to improve statistical power. New technologies, such as next generation sequencing, will help us  identify these elusive obesity-associated variants, particularly as the price of these techniques  continues to drop. 

In addition, most of variants that capture the association with obesity from current  GWAS are not themselves causative. As such, how to move from association to causality remains a  big challenge for common complex diseases like obesity. Therefore, we need to develop new  approaches for analysis to characterize the true causative genes and perform functional studies to  determine their roles in obesity. Once at least some of these challenges have been mastered, we will  have a clearer picture of the genomics of obesity. This, in turn,will help us produce more efficacious  therapies and will guide us on the path to personalized medicine. 

Somehow the basic element of obesity is missed. How does a gene make you eat more? Perhaps you have a lower BMR but the equation holds for almost all humans. Why waste time on genes. One must tell fat people they are fat because they fail to control intake, it is their fault.

Banting and Best, What is the Cause Again?

Banting and Best where are you when we really need you? I am always amazed by authors such as Basu et al who come out with a new discovery regarding sugar and Diabetes. It is as if they have just gotten some clear insight into the obvious. Obesity drives the suppression of the islet cells which drives down the insulin production which drives up the glucose level. Get the BMI below 22.5 and you drive out the main initiator of Type 2 Diabetes, the inflammatory effects of weight.

Now the authors state[1]:

While experimental and observational studies suggest that sugar intake is associated with the development of type 2 diabetes, independent of its role in obesity, it is unclear whether alterations in sugar intake can account for differences in diabetes prevalence among overall populations.

Using econometric models of repeated cross-sectional data on diabetes and nutritional components of food from 175 countries, we found that every 150 kcal/person/day increase in sugar availability (about one can of soda/day) was associated with increased diabetes prevalence by 1.1% (p ,0.001) after testing for potential selection biases and controlling for other food types (including fibers, meats, fruits, oils, cereals), total calories, overweight and obesity, period-effects, and several socioeconomic variables such as aging, urbanization and income.

No other food types yielded significant individual associations with diabetes prevalence after controlling for obesity and other confounders. The impact of sugar on diabetes was independent of sedentary behavior and alcohol use, and the effect was modified but not confounded by obesity or overweight.

Duration and degree of sugar exposure correlated significantly with diabetes prevalence in a dose-dependent manner, while declines in sugar exposure correlated with significant subsequent declines in diabetes rates independently of other socioeconomic, dietary and obesity prevalence changes. …

In summary, population-level variations in diabetes prevalence that are unexplained by other common variables appear to be statistically explained by sugar. This finding lends credence to the notion that further investigations into sugar availability and/or consumption are warranted to further elucidate the pathogenesis of diabetes at an individual level and the drivers of diabetes at a population level.

Well one would think that to be the case. Sugar, sucrose, is a powerful carbohydrate and Diabetes is a carbohydrate disorder, and Type II Diabetes is exacerbated by obesity and sugar has excess calories thus causing obesity. It is logical causality. We have seen genes, billboards, environment, sugar, and endless excuses for the fact that people eat too much.

Most physicians treating Type II Diabetes sees the patient as obese, having a high carb diet, more than likely smoking and with no exercise. Further if they examine the diet, they find tremendous amounts of carbs, and if they look deeper they are dominated by various sugars. Thus this conclusion is not only obvious but it faces physicians on a day by day basis.

The prototypical Type II Diabetic is a candy eating obese person. Instead of a small candy bar, they get bags of them, cakes, cookies, and the list continues. So what is new?

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[1] http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057873

The Cause of Obesity: It is Food Stupid!

There is an article in today's NY Times which states:

OBESITY is a problem everywhere, with significant consequences for personal health and public spending. People weigh more than ever — but why? If we can find the causes of obesity, we can try to eliminate or counter them.  Unfortunately, finding causes is easier said than done, and causes we think we see can turn out to be illusions.

The cause, well simple, it is food. Remember 3500 kcal per pound. You basal met rate is say 2000 kcal per day, you eat 2500 kcal per day you gain a pound a week. Simple, End of story. Do not look any further! Input less output is Net Accumulation.

Now here is a real dumb statement:

The gold standard for inferring causation in social science, as in medicine, is the randomized controlled trial, in which people or places are randomly assigned to receive different treatments. In this case, the “treatment” would be the amount of outdoor food ads in an area. But advertisers are unlikely to agree to randomly distribute their signs, nor would people consent to live in a randomly chosen place.  

The gold standard is simple physics, in this case energy input and output. The author is a psychologist so I guess I should not be surprised. It is food, too much food. Let me give a few examples:

1. A decade ago when I brought my Czech partners and their family to the US I took them to a lunch restaurant. The plates came out and they were shocked, they at first thought one plate was for all, like a family meal, then they realized that one was for each. In Prague at lunch we had a small plate of food, and even 6 oz of beer, not my choice, but all in moderation.

2. At a day recently of lunches and dinners I kept to my bowl of soup while I saw others with fries and piles of food, well in excess of the 2000 kcal per day. It was not pure choice, but it was choosing Item 9 on the menu. I went off menu. No problem, just ask.

3. The typical business lunch in a conference room contains sandwiches that contain not only bread and meat but a collection of calorie adding stuff. The solution, remove the bread and stuff. Stick with the protein. Also there is always the soda and deserts. Hands off!

The "cause" of obesity is obvious, more input than output. The more I speak with people the more I am concerned the only way to stop it is through taxation, pure and simple. Especially if those who opine like those in the Times are totally clueless.