Still Rethinking Hypothyroidism

Last week’s podcast introduced a new concept – the concept of leptin resistance being the predominant hormonal cause of having a low body temperature. This of course, is not the only cause. Having low levels of leptin like that of an anorexic will certainly manifest in the form of low body temperature just as high leptin levels in someone with low leptin sensitivity will.



If your thyroid gland truly doesn’t work like it should, or the TSH signals coming from the pituitary aren’t functioning well, then you’re likely to have a low body temperature as well. This probably has absolutely nothing to do with leptin.

But having hypothyroid symptoms, or having a low body temperature – the gauge used to diagnose hypothyroidism by Mark Starr, Stephan Langer, and Broda Barnes, does not mean you are hypothyroid. In fact, the reason there is such controversy over the issue is that endocrinologists are testing for thyroid hormones and often find that they are totally normal or very close to it – even when a hypothyroid diagnosis seems so certain.

Yes, your thyroid gland is no doubt underperforming if you have a low body temperature. But that doesn’t mean that your thyroid gland is the problem. It may just be taking orders from the boss.

In a brief e-mail conversation with Stephan Guyenet of http://www.wholehealthsource.blogspot.com/, another blogger who has put leptin front and center in his current obesity research, Stephan notes that “leptin resistance seems central” to the cause of many related health problems. It certainly does. Here’s why.

Leptin, a hormone that resides in adipose tissue and communicates with the hypothalamus, is kind of like that one pirate that has to sit up high and watch out for stuff like icebergs. You know, the one that yells “Land Ho!” Or maybe leptin is like one of those meerkats that stands on lookout. In other words, leptin is on the outside judging what’s going on, and reporting back to the rest of the system with updates. Leptin is the hormone that provides the body with all its very important energy-regulating feedback.

Leptin’s natural function, when body fat stores decrease like they might during a famine, is to signal to the body that it needs to go into hibernation mode to preserve energy. It also sets in motion a series of hormonal events that favor fat storage, inhibit fat burning, etc. To preserve energy, the body temperature falls. The pulse rate falls. Energy levels plummet. And of course hunger goes wild. It’s a great system really. It’s what keeps our body weight balanced from year to year no matter how much we exercise or how much we eat. It is a self-regulating system with an amazing design (assuming it's working correctly).

When body fat stores increase, the opposite sets in. Leptin’s job is to let the body know that fat stores have been topped off, the famine is over, and signal that the body can get back into its optimal high-performance state. That is a hypermetabolic state, with a high body temperature, lots of energy, quick mobilization of fat in the blood and tissue for fuel, and moderate, more well-controlled appetite that is not seeking to add body fat or exceed maintenance calorie levels – just replace lost calories burned up by physical exertion and metabolic activity.

In a healthy human being that is not leptin resistant, leptin does its job with miraculous exactitude, and body weight is often maintained within a few pounds over the span of decades. The balance sheet between calories consumed and calories burned maintains perfection. Throughout the year weight does not change despite consuming upwards of 1 million calories. Now that is one hell of a good accountant.

The big question that needs answering, and one that can make the greatest impact on reversing metabolic syndrome – a constellation of health problems, each of which is related to leptin’s response to starvation (such as insulin resistance, rising blood sugars, fat storage, taking in more calories than are burned, low body temperature, accumulation of blood fats, and hypercholesterolemia), is “What causes leptin resistance?”

Fructose researcher Richard J. Johnson is very adamant that fructose is central to leptin resistance. This article was released in October of 2008 at http://www.medicalnewstoday.com/ and may be of great significance:

Could all those years chewing candy and slurping sugary sodas come back to haunt you? Perhaps. A new University of Florida study in rats shows that a fructose-filled diet blocks the appetite-controlling hormone leptin from doing its job, setting the body up for future obesity.


Leptin is critical in controlling appetite and energy expenditure, and scientists have long linked leptin resistance to obesity. And several studies have shown that overconsumption of fructose, a sugar found in everything from apples to cookies, could be playing a significant role in the obesity epidemic. But the UF study, recently published in the American Journal of Physiology - Regulatory, Integrative and Comparative Physiology, is the first to link fructose and leptin resistance.


UF researchers found that rats became resistant to leptin after being fed a diet high in fructose for six months. Although there were no visible signs this change was occurring, the fructose-fed rats gained considerably more weight than rats that never ate fructose when both groups were switched to a high-fat diet.

"Leptin resistance is a condition that leads to obesity in rats when coupled with a high-fat diet. The surprising finding here was that increasing the amount of fructose in the diet without increasing the amount of calories led to leptin resistance and later exacerbated obesity when paired with a high-fat diet," said Philip J. Scarpace, Ph.D., a professor of pharmacology and therapeutics in the UF College of Medicine and the senior author of the study.


According to this study's findings, fructose itself does not cause obesity, but alters the way leptin works.
"It blocks leptin action most likely by blocking leptin entry into the brain," said Alexandra Shapiro, Ph.D., an assistant scientist in the department of pharmacology and therapeutics and the lead author of the study.


To test how fructose affects leptin, the researchers studied two groups of rats. The rats in both groups received the same number of calories each day, but one group received chow containing 60 percent fructose while the other was kept on a fructose-free diet.


"After six months, we could not detect any differences between the two groups of rats, with the exception of an elevation in blood triglycerides in rats on the high fructose diet," Shapiro said. "They had identical body weight and fat, as well as blood levels of leptin, insulin, glucose and cholesterol."


But when the researchers tested how the two groups of rats responded to leptin, they discovered that the rats eating fructose had become resistant to the hormone, while the other group of rats responded normally.


"From an overall point of view, what this study shows is that fructose, in high enough concentrations, can induce leptin resistance, and it could implicate dietary fructose as a potential risk factor for human obesity," said Joseph Vasselli, Ph.D., a research associate at the Obesity Research Center at St. Luke's-Roosevelt Hospital Center in New York and a research associate scientist at Columbia University.


Typically, leptin resistance develops with obesity, but this study showed that high dietary fructose causes a "silent" leptin resistance, Shapiro said. It develops undetected, but when the high-fat diet is introduced it causes greater than expected obesity.


"Fructose sets you up," Scarpace said. "If these findings are applicable to humans, then there could be consequences of eating a diet high in fructose, but only if you also consume an excessive amount of calories. If you go on a trip, attend a celebration, or otherwise eat more than you usually eat, a person consuming a low-fructose diet may be able to handle it. But the individual who has set themselves up so that leptin no longer works will be unable to burn the extra calories, and now they gain a lot of weight."


The current findings only apply to rats, of course. Studies in humans have yet to confirm the role of fructose in leptin resistance.


Vasselli, who wrote a commentary about the UF study in the journal, said the findings could also help researchers study leptin resistance in humans.


"I think this is a very important study," Vasselli said. "It raises a lot of issues that have to be investigated. It shows this is one way leptin resistance can happen."

Of course, one thing the article ignores is that being leptin resistant is likely to make you want to eat more calories. Leptin is, after all, the hormone in control of appetite.

Another thing that is potentially of great significance is that the fat given to rats on a “high-fat diet” is almost invariably corn oil – a highly concentrated source of omega 6. Leo Galland, author of The Fat Resistance Diet feels like inflammation is the cause of leptin resistance, and we know what role corn oil might play in causing a hyperinflammatory condition in the body.

And thus we’ve come full circle. “Do not combine a lot of fructose with a lot of polyunsaturated fat in your everyday diet.”

And there is still some indication that the polyunsaturated fatty acids are a larger player in creating a hypometabolic state than fructose. This article about increasing the metabolism through polyunsaturated fat restriction by Ray Peat is certainly intriguing.
http://raypeat.com/articles/articles/unsaturatedfats.shtml

But one thing remains clear and very promising. If there’s one thing that the controversial practice of low-fructose overfeeding advocated here can do, it’s raise the body temperature. If Broda Barnes’s modern-day followers are diagnosing hypothyroidism on the grounds of a low body temperature, and we are bringing up body temperature with many corresponding health improvements related to overcoming a sluggish metabolism, then clearly we are on to something significant.

My own body temperature has risen from 96.2 degrees F to 97.7 degrees F in the last three months as part of my rehabilitation from overexercising during the summer of 2009.  And that seems to be a typical response. 

Yes, Broda Barnes's modern-day advocates are changing people’s lives by overriding low metabolisms. They should be commended, and it’s probably better to have a high metabolism with desiccated thyroid help than to remain hypometabolic. But it may not be getting to the root of the problem, and the answer to clearing it up may be much simpler – eat the food!

Don’t reach for the desiccated thyroid yet. Make sure it’s really your thyroid gland that can’t get the job done before you go there. If you are already on desiccated thyroid, you might want to eat well and wean yourself off of your medication if you start to display hyperthyroid symptoms.