Still Rethinking Hypothyroidism

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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.

30 Comments

  1. Nice. @ Matt:

    "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. "

    I am interested too hear what exactly your over exercising was as well as what symptoms you were feeling? plus how much weight did you gain in order to get your Body Temp up?

    Keep up the great blogging some really cool stuff you are rolling out…

    Reply
  2. My weight peaked 19 pounds above my post-exercise level, and 14 pounds above my peak weight prior to over-exercising. This is typical of prolonged calorie deficit.

    I was short on cash and had to work another season with the Forest Service as a Wilderness Ranger, a job I've done off an on since age 19.

    It involved about 30 hours of high-intensity hiking carrying lots of weight, tree cutting with hand tools, and trail work each week. An estimated calorie burn of at least 20,000 calories in addition to basal calorie burn. I tried to eat as much as I could, but found it to be impossible.

    Symptoms weren't bad, but I had typical hyperphagia, constipation and skin breakouts upon ingesting more food, rapid fat gain, low body temp., low pulse, low blood pressure, low sex drive, fatigue, etc.

    But weight peaked and has dropped 4.5 pounds since 1/1. I feel awesome, and all original symptoms are gone.

    My blog post on Thursday will put this weight fluctuation into perspective.

    Reply
  3. Matt, got a list of therapies that have proven wildly successful at healing/improving leptin sensitivity? Is HED still the best?

    Also, I've been reading about iodine lately and there's a lot of conflicting information on proper dosing. I'm sure I do okay, since I drink a lot of milk and eat potatoes and eggs (all good sources), but I'm not in the mg/day camp like the Japanese. Thoughts?

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  4. Great post!

    I guess there's not a cheap and easy way to tell if I have thyroid problems or leptin problems or both. I am very overweight but I gained all of the excess weight in one year of eating normally after two years of being bulimia. Do you think bulimia would be more likely to damage the thyroid than cause leptin problems?

    Reply
  5. you are doing such a great job on this research on leptin! I'm not sure if this is one of your interests, but I would be interested in hearing your thoughts on the effect of SSRIs or other psych meds on leptin. I gained over 70 pounds taking an SSRI, and I suspect that how it was caused might have been some kind of interference with leptin, since the drugs are processed through the hypothalamus. With the number of people taking these drugs, this could affect a lot of people.

    Reply
  6. Absolutely. The SSRI connection with weight gain is very interesting, and something I hope to get deeper into in the future. Serotonin and insulin levels are very intimitaley correlated.

    April-
    Gaining weight after being bulemic is no shocker. There may be nothing wrong with you at all that can't be healed by eating well. That's my hunch.

    Brock-
    Leptin is a relatively new discovery. Very little is known about what causes leptin resistance. But clearly, as you have demonstrated, overfeeding and resting can bring up the basal temps, bring fat gain to a halt as temps peak, and reduce hunger as weight starts to creep downward.

    Reply
  7. How does "SAD > liver insulin resistance relative > hyperinsulinemia > fat cells less resistant than liver so the high insulin levels cause excess fat deposition" fix into all of this?

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  8. Matt:

    "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"

    You didn't mention low grade inflammation which seems to play some role as well. Inflammatory responce of the body may be even one of the most important players here.

    I really loved that Ray Peat link, thanks! Omega-6 fats are often been referred as a cause for inflammation but I still quite disagree because even if omega-6 will exaggerate immune responce to inflammatory stimuli it still is not a causative factor. For example LPS is.

    I think all "metabolic dysfunction markers" including leptin resistance or increased cortisol could be explained by inflammatory responce of the body which is related to how body work under the situations of (prolongued) stress.

    http://www.ncbi.nlm.nih.gov/pubmed/18926322

    If fructose feeding increases leptin resistance it might do it by activating immune system some how. Maybe in the gut or liver? That could explain also why fructose feeding increases fatty acid release from the adipose tissue.

    I'm sure we will eventually figure this all out…thanks for the good work Matt!

    Reply
  9. I sure hope to be a happy test case for weaning off of thyroid meds, although I expect that would be years down the road. Thyroid stuff is a sore subject for a lot of us at the moment, because there's a huge shortage of dessicated thyroid thanks to govt. intereference — I've had to go on synthetics, and I'm sure a lot of others have too. Sucks!

    I'm just digging into Kharrazian's "Why Do I Still Have Thyroid Symptoms?" Pretty good so far. Much emphasis on getting the immune system working right, correcting TH imbalances, etc. He's not a fan of simply giving meds until the labs look right, but going for a deeper healing.

    Also he's saying iodine is bad news for anyone with Hashimoto's, which is pretty common for peeps with thyroid problems. Not sure what to make of that yet.

    Reply
  10. Trix-

    Yes I did read it, and both Joe Blair and I commented on it. Going to a WAPF conference was a real wake up call for me. Their info. is a step in the right direction for humanity in general, but it was plain to see how ineffective their information was at solving serious health problems. Since then, I've questioned why that may be and have explored "specific dietary strategies for specific disorders."

    Westie is right. Most of this will come back to inflammation, and inflammation does appear to be central. I have a gut feeling that WAPF followers would have much better health improvements and greater vitality and longevity if they were to target the inflammatory imbalance specifically and aggressively. Instead, they advocate one of the most inflammation-promoting diets of all – one rich in the highest sources of dietary AA with other huge powerhouses of omega 6 as linoleic acid (from nuts, poultry fat, lard, etc.).

    Anonymous-
    Insulin resistance is something I believe to be, just like increased hunger, decreased energy levels, and lowered body temperature, to be an adaptation to starvation. Being leptin resistant or having low leptin levels would both induce insulin resistance in response to food.

    The question is what causes leptin resistance? The key dietary association is with fructose, and history shows that the introduction of refined sugar to be the most menacing dietary constituent in degrading human health. But inflammation is central to the whole issue, and it would seem impossible for omega 6 not to be involved somehow.

    Reply
  11. And once again, to go Barry Sears on you guys, remember that for omega 6 to become converted to hyperinflammatory Arachidonic Acid, it requires hyperinsulinemia to trigger an over-activation of the delta 5- Desaturase enzyme.

    So it could just be that fructose, and also excessive caffeine and excessive alcohol induce insulin resistance (probably via inducing leptin resistance), triggering the delta 5-desaturase enzyme to manufacture AA instead of non-inflammatory DGLA out of the omega 6 linoleic acid we ingest.

    In other words, fructose could be the primary culprit in creating all this inflammation, and that would make sense looking at the work of T.L. Cleave for example, who noticed all the facets of metabolic syndrome on a low-fat diet with little, if any vegetable oil.

    But one can probably make huge leaps in health by eliminating one or the other completely – either fructose or dietary omegaa 6.

    Once tissue concentration of omega 6 had been reduced, one could "get away" with eating sugar. This may be the explanation linking Ray Peat's findings to mine, even though they seem incongruous.

    The theme remains. Don't eat fructose and polyunsaturated fat together. That is "the perfect nutritional storm."

    Reply
  12. Hey Matt, not to get off-topic here (well, not too far, anyway), what's your take on how to apply HED concepts when you're sick…meaning, of course, sicker than the general state of malaise that most of us who hang out here live in on a daily basis. I've never been able to keep the feeding/starving colds & fevers thing straight…is there any value to either approach when you're nursing a bug? Should you eat if you're not hungry? Eat more? Eat less?

    Any clue?

    Reply
  13. April,

    The Nutrimeds stuff is only T3. Armour and Nature-Throid, rx only, are about 94% T4 and 6% T3, something like that. I considered getting synthetic T4 and adding in Nutrimeds, but my doc convinced me to go with a compounded med so we could fiddle with the ratios. I'm just hoping production ramps up soon and I can go back to Nature-Throid. As a step towards getting off altogether of course!

    Matt,

    One of my favorite things about your work is the focus not on "what's a great diet?" but "what's a great diet for fixing metabolism and healing all the body systems?" I don't see anyone else working on this.

    I think gluten fits into that distinction because for people with gut problems (the majority?), it makes the situation way worse, triggering adrenal burnout and inflammation, making it that much harder for the gut to absorb all the good stuff we're cramming in there. But that's not to demonize wheat, since if you aren't intolerant it can be a helpful and tasty food. I'm looking at exclusion as hopefully a temporary measure, though not a short-lived one sadly.

    I've been totally off sugar since New Year's Eve. Last night I made some roasted butternut squash (with a ton of butter) and it was almost too sweet to eat. Like candy!

    Reply
  14. Thanks, Matt….I didn't go all the way down the page so I didn't see the comment you left. Makes sense. I think your right about controlling inflammation as being central.

    I read some about the Vit D dysregulation but a lot is a bit over my head. Is it basically saying that f you are already diseased and unhealthy then Vit D supplementation can exacerbate the situation and not help?

    Reply
  15. Trix-

    After further exploring the vitamin D issue it seems that the Marshall Protocol is pretty dumb, dangerous, and purely theoretical. It was interesting to see that there is a such thing as vitamin D receptors, meaning that intake is only part of the story.

    Nell-

    Thanks for that. I know this is one of the greatest strengths of this site. To argue about what is and isn't a healthy food from a list of foods that have been staples of healthy human groups for thousands of years is a monumental waste of time. Now it's time to go beyond that and find specific strategies that target specific disorders. That is the real power of nutrition in preventing and reversing disease.

    Reply
  16. If someone has the autoimmune disease , hashimotos, do they have to use thyroid replacement then? since its the thyroid thats being attacked and acting slowly?

    Reply
  17. Solid post.
    Good job on the "All Newcomers, Read this first" overview. Very comprehensive and as concise as possible. It will help the old timers as well as newcomers I suspect.

    Reply
  18. Sarah, a guy like Charles Sanford Porten would have said: if fever, fast, if chronic, eat.

    Rice burner

    Reply
  19. Thanks Rice Burner and Lisa.

    On Hashimoto's, that is very different than just having a "sluggish metabolism." In most cases it does lead to necessary thyroid hormone supplementation.

    Reply
  20. Ran across this today doing some researcha nd hope to get some feedback. All thyroid levels (tested 5 times in the last 2 years) are WNL. However, I experience all of the symptoms:
    Fatigue
    Hair falling out/curly
    Chronic constipation
    Yellow/pale skin
    Cold/intolerant to cold
    Low heart rate (45)
    Ceased periods
    Bad reaction to BC pills
    Low/no sex drive
    Dry skin & brittle nails
    Slowed gastric motility
    Phytobezoar

    I consistently have lower than 98.6 when measured, but will start consistently monitoring tomorrow morning. I am female, 5'7" ~140, 17-20% bf, weights 4 days/week, cycling 2 hours/week.

    Struggling with the idea of no exercise for 30 days, but realize 30 days is nothing if things begin to normalize. Thoughts, ideas, observations?

    Reply
  21. Hi Amanda-

    Let's see those morning temps. I'm sure they will come out quite low.

    Have you lost a lot of weight from a former heavier version? Just curious. The more details of your diet history, health issues of other family members, etc. the better.

    Reply
  22. Started dieting and exercising about 7 years ago and didn't so much lose a lot of weight (maybe 10-15 lbs) but changed body comp considerably and became very muscular, therefore much leaner. I also lost my cycle about 6 years ago.

    Started with Atkins, then BFL, then CKD, then did Eat-Stop-Eat for about a year, then just random IFing, and now paleo/primal for the last 5 months. Diet has consisted of lean protein, healthy fats and boatloads of fruits and veggies, which, I believe, have contributed to my food baby (bezoar). I was just diagnosed with that last Friday so I am cutting fruit, limiting veggies and watching my fiber intake.

    Family history of heart disease and fibromyalgia. Also just had CBC done: LDL 197/HDL 93. (another possible hypothyroid symptom).

    I will start tracking body temp tomorrow.

    Reply
  23. People are often confused because they equate leanness and muscularity with health. In actuality, leanness and muscularity, while it may be something that a lot of healthy people display, isn't necessarily something that delivers health to someone who was formerly flabby.

    In fact, decreasing body fat is often times enough to eradicate a woman's period. Not having low body fat, but just decreasing it, which lowers leptin levels and catapults a person into hibernation mode.

    Protein really aggravates low-metabolism issues as well. You'd fare much better with a total reversal in my view, really stressing high fiber carbohydrates, calories, and rest and limiting protein and fat and exercise.

    I also wouldn't spend much time fasting either. This may be something a healthy person can do, but it's not something an unhealthy person can often get away with.

    Reply
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  27. Hypothyroidism can also be managed with natural thyroid support with supplements.The truth is, there are natural methods of dealing with hypothyroidism, and there are also supplements available to boost the effect of natural thyroid support.

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  28. Hi there! This post couldn’t be written any better! Going through this post reminds me of my previous roommate! He continually kept talking about this. I am going to send this post to him. Fairly certain he’ll have a very good read.
    Thank you for sharing!

    Reply

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