Is The Biggest Loser Bad for America?

Is the TV show The Biggest Loser bad for America?  Does it portray unrealistic results that are in fact going to discourage people from doing the hard work necessary if they’re going to lose weight?  Are the contestants put into life-threatening situations?  And what does all this have to do with Triple H?

I wrote up a full article on my fitness website here about it.  But, the connection to this site is that obesity  is fascinating from an evolutionary  and cultural standpoint.  We are the ONLY primate that has an obesity problem (when was the last time you saw a fat baboon?).  There are other fat animals on the planet, sure, but they are rather different  from us, and all of them have a good reason for their weight gain.  Some, like whales need it to stay warm in cold water.  Others, like hippos, use it for buoyancy.  We don’t have a good reason.  The only exceptions in the animal kingdom are domesticated pets–that WE feed too much.

They need a biggest loser for pets

For all the hype and craziness, the show makes it clear that losing massive amounts of fat is  possible.   It will be hard, very hard, but it is possible.

Before the recent past, the only overweight people on the planet were rich people.  Before civilization, when there were no rich people, there were no overweight people either.

The cat on the left has a similar history.   Felines are not fat by nature.   But, given enough food, and a sedentary lifestyle, anything is possible.

The real question for us as a species is, then, how do we alter our culture enough so that obesity ceases to be the norm.  That is, if we live in a cultural and physical environment now that increases (by a lot) the likelihood that you will get fatter as time goes on; then how do we change it.  And to what?

Self control is not enough of an answer, though, on the individual level, it is a good place to start.  I think we need to build better institutions–far better PE programs in school would be a huge start.

We went through nearly 20 years of people telling us that the problem is genetics.  If your parents were fat, then you’ll be fat too.  Not only is that bullshit, but it’s demotivating.  (Of course, genes for fat storage exist, but that doesn’t mean you were doomed from birth.)  How are you supposed to get motivated to get into the gym and to eat healthier if you’re told it is probably genetics, and therefore, there is nothing you can do about it.

The show makes it clear that you CAN lose the fat.  Even if they are doing some wacky stuff, huge people are losing a lot of weight.  And that is inspirational.  Hype or not.

HIV and the T Cell Life Cycle

In an excellent review of a paper in the Journal of Biology (“Generalized immune activation as a direct result of activated CD4+ T cell killing“), Nienke Vrisekoop , Judith N Mandl, and Ronald N Germain discuss the life and death of the T lymphocyte.

T lymphocytes have a difficult existence. As mature cells, they are essential for immunity to infection, but in the early stages of their development in the thymus, more than 90% of them fail selection for the appropriate antigen receptors and die before export to the peripheral immune system. Those that achieve maturity spend weeks, months or even years circulating through the body, in constant search of a foreign antigen that their antigen-specific receptor can recognize, and needing continuously to compete for trophic signals necessary for their survival. Most fail to find an antigenic match and remain as small resting cells until death. A few encounter the right partner and undergo a transient bout of exponential clonal expansion, only for more than 90% of these progeny to be lost by apoptosis shortly after the antigen is cleared. The remaining 10% are maintained as memory cells (Figure 1), conferring lasting protection.

Understanding the mechanism of T cell death is a major concern when confronting HIV and its progression into full blown AIDS.

Although it is known that HIV kills activated CD4⁺ T cells, it is still a major unresolved question why these cells progressively decline after infection. It is clear that in infected individuals, the rate of loss of CD4⁺ T cells is greater than the rate of production so that the CD4⁺ T cell pool is gradually eroded over time, but it remains to be determined how the balance between these processes is impaired. It is unlikely that direct killing of infected target cells by HIV is sufficient to cause CD4⁺ T cell depletion. Natural hosts for simian immunodeficiency virus (SIV), such as sooty mangabeys, do not progress to AIDS and maintain near-normal levels of peripheral CD4⁺ T cell numbers despite high rates of viral replication [4]. In fact, the level of immune activation is a better predictor of disease progression than viral load. Consistent with this, HIV infection in humans leads to chronic generalized immune activation characterized by an increased rate of exit of CD4⁺ and CD8⁺ T cells and of natural killer (NK) cells from the resting state, increased T and NK cell turnover and death, polyclonal B cell activation with increased levels of gamma globulins, and elevated production of pro-inflammatory cytokines. Conversely, chronic immune activation is not seen following SIV infection in natural hosts that do not show progression to AIDS [4].

That is, there is a question as to what causes the autoimmune response that is so devastating to people with AIDS.  There are two proposed methods of activation.  The first is that chronic activation of the hosts immune system disrupts CD4+T cell homeostasis.  The second is the opposite, that HIV drops the CD4+T count out of homeostasis and the bodies over-active response is chronic immune activation.  The authors make the point that these two possibilities are not incompatible.

Clearly, the two possible causal relationships between chronic immune activation and CD4⁺ T cell loss are not mutually exclusive. In fact, chronic immune activation and the loss of CD4⁺ T cells may amplify each other in a loop that makes it difficult to establish which process underlies and drives the other.

The study in review attempted to induce this same response in mice.

Marques et al. [1] suggest that the OX40-DTA mouse is one approach to this issue and that the findings in these mice provide important insight into the control of lymphocyte dynamics in infected humans. Indeed, in the absence of exogenous infection, OX40-DTA mice do show features consistent with generalized immune activation (Table 1), including an expansion of effector CD8⁺ T cell numbers that inverts the usual CD4⁺:CD8⁺ T cell ratio, and increased serum levels of inflammatory cytokines. This generalized activation cannot be attributed to the release of microbial components into the circulation from the gut, because deletion of activated CD4⁺ T cells does not in itself lead to a breach in the gut epithelium. Notably, Marques et al. [1] show that the expansion of effector CD8⁺ T cells and increases in serum levels of inflammatory cytokines can be reversed following reintroduction of Tregs from normal mice, suggesting that the increased immune activation in OX40-DTA mice can in part be ascribed to a Treg insufficiency, which they propose is a key event in HIV-infected individuals leading to CD4⁺ T cell depletion.

There’s a lot more, and the review goes into much more detail.  But, I can see how this approach could be fruitful in illuminating the underlying causes of a disease that plagues such a large number of humans on the planet.