Not enough, rather than too much fat, causes metabolic problems of obesity

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That’s right – contrary to what many religiously believe, it is the inability to grow more fat during times of energy surpluss, rather than the excess of fat which appears to directly contribute to the metabolic consequence often associated with obesity.

An article in the New Scientist shines some light on this issue;

Obesity kills, everyone knows that. But is it possible that we’ve been looking at the problem in the wrong way? It seems getting fatter may be part of your body’s defense against the worst effects of unhealthy eating, rather than their direct cause.

While the article goes on to discuss some interesting new research, I feel the author misses an opportunity to really challenge the overwhelming dogma that too much fat, per se, is the cause of metabolic consequence of obesity. From my experience, it is much easier to get the point across by investigating the obvious anomalies or outliers to the often thought direct relationship between excess adiposity and disease.


Outlier #1: Lack of adipose tissue leads to severe metabolic abnormalities

Individuals who suffer from a condition called lipodystrophy, have little to no fat tissue (they look extremely athletic, with defined musculature) but display many of the metabolic symptoms thought to be exclusive to obese individuals. Lipodystrophy encompasses a heterogeneous group of disorders associated with whole body or partial lack of adipose tissue, which can be inherited (genetic-origin) or acquired. Not only are patients with lipodystrophy at increased metabolic risk, but the severity of metabolic complications observed is closely related to the extent of their fat loss.

Outlier #2: Excessive growth of adipose tissue leads to healthy metabolic profile

The opposite clinical example of lipodystrophy is multiple symmetric limpomatosis. Multiple symmetric lipomatosis represents a group of similar syndromes characterized by the excessive growth of subcutaneous fat, often in the periphery of the body in areas such as the arms, legs, shoulders, and neck (picture the Michelin man). For a given BMI, multiple symmetric lipomatosis patients are reported to carry 50% more fat tissue than healthy individuals. Interestingly, numerous case studies have found excellent metabolic status (high insulin sensitivity, normal glucose tolerance, normal blood lipid levels and blood pressure) among these individuals despite their obviously obese state.

Outlier #3: Liposuction of adipose tissue does not lead to metabolic improvements

If merely the amount of excess fat is the direct cause of metabolic dysregulation then removing that fat through surgery should obviously result in metabolic improvement. Unfortunately, this is not the case. In fact, an excellent prior study has shown that liposuction does not make obese individuals healthy.

Outlier #4: Pharmacological treatment of unhealthy obese individuals leads to increased adiposity in concert with improvement in metabolic profiles.

All of the above examples would seem to suggest that if obese and metabolically unhealthy individuals could somehow develop more subcutaneous fat tissue, they could theoretically become healthier.

Guess what? That’s exactly what happens!

Obese individuals with metabolic problems who are prescribed a class of drugs called thiazolidinediones or TZDs for short, actually grow more fat cells, get fatter, but also get healthier.

Currently, the emerging theory of why obesity is associated with metabolic disease risk suggests that it is not the excess amount of fat that results in problems – but rather, it is the inability of the fat tissue (specifically subcutaneous) to expand enough via the development of numerous, healthy adipocytes or fat cells to store all the excess calories being ingested (more details on that here).

The mantra that “fat is bad” is not only myopic, it now stands in the face of much contradictory evidence. As the examples above illustrate, matters related to excess fat and health risk are much more nuanced than what many would have you believe.

Finally, while I only discussed issues related to metabolic health, it is also proposed that the association between excess fat and other conditions such as osteoarthritis, sexual dysfunction, and cancer may also be more closely tied to the function rather than merely the amount of fat in one’s body. These notions are nicely summed up by Dr. Harold Bays’ adiposopathy theory, which has been getting more traction over the years as more supporting evidence emerges (check the reference below). Alas, this may be an issue for a future post.

Peter Janiszewski

Bays, H., & Dujovne, C. (2006). Adiposopathy is a more rational treatment target for metabolic disease than obesity alone Current Atherosclerosis Reports, 8 (2), 144-156 DOI: 10.1007/s11883-006-0052-6

Today’s post was originally published on March 19, 2010, during our time on Scienceblogs.

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6 Responses to Not enough, rather than too much fat, causes metabolic problems of obesity

  1. Pingback: How do fat cells protect you from metabolic risk? | Obesity Panacea

  2. A. says:

    On the topic of the dangers of too little adiposity, I would love to see you do a post on the physiology of weight restoration and “refeeding syndrome” in people recovering from anorexia or other forms of starvation.

    • Travis says:

      Excellent idea! I’m not aware of many studies on recovering from anorexia (although that may be due to ignorance rather than a lack of actual research in that area), but there are some really fascinating studies on the re-feeding of starved populations following WWII.

  3. Steve says:

    Good article, and I agree – the body weight/adiposity debate requires much more investigation and – unfortunately for public health messages – nuance.

    Across the population, the BMI-disease relationship is still robust. Clearly, this doesn’t provide insight to the pathophysiology and it certainly doesn’t explain the relationship in individuals, notably the outliers. Indeed, BMI seems to be a proxy (or confounder depending on your perspective) for something else (visceral adipose tissue [VAT], most probably).

    Whether VAT is the cause of these metabolic effects or is another consequence (ie marker) of an underlying metabolic disorder remains unclear, but it seems that the evidence is now favouring the latter.

    Finally, I think the the headings for outlier one and two are misleading, specifically the verb “leads”. It is lipomatosis and lipodystrophy that leads to the fat distribution and the metabolic consequences – ie, common antecedent.

  4. majkinetor says:

    Awesome post. Thanks.

    Could this explain why slightly higher BMI (between 25 & 27) has the lowest mortality rate .

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