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“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
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Sunday, March 22, 2015

Does Metabolic Syndrome hamper weight loss efforts?

BUMP:  This post is over four years old (original publish date:  11/17/10).  It came to mind a day or so ago when someone linked me to Sam Feltham's latest DISinfographic and accompanying video.

If what Feltham is saying (and I can't for the life of me understand how he "borrows" this from Bailor w/o any complaint from Bailor ... even his book title is similar to Bailor's former one!), the results in this study shouldn't have occured.

So the original (short) post, unedited, and some commentary afterwards in how some things have changed in my knowledge, understanding and thinking about all of this.


This study would indicate that, if anything, it helps (??Say what!!??)

Does the Presence of Metabolic Syndome Influence Weight Loss in Obese and Overweight Women? (PDF full text free until end of the month)
Background: It is known that weight loss is benefi cial for obese and overweight subjects with metabolic syndrome. Very few data exist, however, about whether the presence of metabolic syndrome and insulin resistance (IR) infl uence the response of these subjects to weight-reducing interventions. The current study intends to examine whether the presence of metabolic syndrome and its components could infl uence weight loss in obese and overweight women during a short-term, dietary-based intervention program.

Methods: A total of 107 women aged 49.1 ± 13.5 years old, with a body mass index (BMI) greater than 25 were studied. The subjects were prescribed a low-fat diet plus weight-reducing drugs when necessary.
Results: After 3 months, the subjects with metabolic syndrome lost more weight than those without (6.62% vs. 4.50%; P < 0.05). There was a positive correlation between the percentage of weight loss and the number of the components of metabolic syndrome present at baseline (Spearman ρ = 0.329; P < 0.01). Furthermore, patients in the quartile with the highest homeostasis model assessment index (HOMA-index) lost more weight than the remaining subjects (8.17% ± 3.34 vs. 5.59% ± 3.87; P < 0.05). These results were signifi cant, even after adjustment for the medical treatment prescribed.
Conclusions: Obese and overweight patients with metabolic syndrome showed a greater reduction of their body weight, compared to the patients without metabolic syndrome. The components of the metabolic syndrome present at baseline correlated positively with the percentage of the weight loss. Finally, the patients with the highest levels of HOMA-index at baseline lost significantly more weight than those with lower levels of this parameter.
I find this somewhat surprising.  It would seemingly go counter to what one expects given the effectiveness of low carb diets and how an even higher fat lower carb/protein version (e.g. fat fast, Silver Cloud Diet) is usually advocated for the more hyperinsulinemic.  This study looked at a low fat diet.  One would also think that if insulin resistance (which is the underlying factor in metabolic syndrome) causes obesity then the obese/overweight with IR should have greater difficulty losing weight.  

Things that make you go hmmmmmm.


For those who are newer to the blog, and/or perhaps the low carb community, etc., the atmosphere in 2010 was still dominated by vocal proponents of what I call TWICHOO:  Taubes Wrong Insulin-Carbohydrate Hypothesis Of Obesity.  Ketomania was yet to be launched, but the "up the fat" if you were stalled was common advice, as was the notion that fat couldn't make you fat so long as you didn't eat carbs with it.  People were still convinced that calories didn't count at all (most at least acknowledge that they do, at least when pushed in debate) .

But most importantly, the Taubes part of TWICHOO which was the progression of insulin resistance dominated.   There is overwhelming scientific evidence that peripheral (muscle cells) insulin resistance may not even exist!  Whatever slight impairments in glucose transport are attributable to a reduction in GLUT4 transporters, and glucose clearance is not impaired in type 2 diabetics.  If you haven't already read this blog post, may I suggest it as future reading?   The Cause of Hyperglycemia in Type 2 Diabetes.

Taubes progression:
carb ingestion → insulin secretion ... high carb ingestion → more insulin secretion → chronic hyperinsulinemia → peripheral insulin resistance → fat accumulation → eventual adipose insulin resistance

is not supported by either observation or pretty much any interventional evidence.

Probably for at least the past year, I've used the term insulin resistance much less frequently.  Unfortunately the whole hormonal resistance idea is so ingrained in the lexicon that it cannot be replaced.  If this is so, then it needs to be re-defined to correspond to the scientific evidence.  What is often perceived as IR -- and makes "common sense" = a back-up of glucose into circulation -- is actually due to a loss of initial insulin secretion and glucagon suppression leading to unchecked glucose production in the liver.

Where this ties in with this study, is that low carb proponents still cling to this idea and claim this is why "low fat high carb diets don't work".   This is simply not the case.  When you become obese, your metabolic milieu certainly changes.  Some of this may be irreversible, or at least persist for years following loss of the weight.  But it appears that -- barring an underlying serious endocrine/genetic disorder -- the "damaged metabolism" of this nature does NOT stand in the way of weight loss.  And just to be clear, I don't put a whole lot into any greater weight loss observed in this study in the more metabolically deranged, but it is an outcome that flies in the face of the "alternate hypothesis".


Mario Renato said...


Excuse my ignorance, but this was not exactly what one would expect? If you are overweight, but your body is not being damaged, it's not logical to think that it would try to keep this fat?

CarbSane said...

Mario, what you say makes sense. If one thinks "metabolically", it would seem logical that the body would want to get rid of fats that overfill our capacity but have less of a reason to rid itself of fat that is within our storage capacity and not doing damage as you say. What I mean about this result being "not expected" is that in Atkins, and carried on by his proteges today, there is mention of those that have difficulty losing weight even on low carb -- the metabolically resistant. This resistance is attributed to hyperinsulinemia which is a result of insulin resistance. The more MetS markers the more weight lost on a high carb/low fat diet, and it is reasonable to presume that these correlate with the degree of hyperinsulinemia. So these results are counter to what might be expected vis a vis LC theories.

Kindke said...

1000 Calorie deficit is alot though. In my experience even on a ketogenic diet weight loss eventually stalls unless you start to cut calories alot.

I would expect insulin resistence to quickly correct itself in a semi-starvation diet even on 200g carbs per day.

Nigel Kinbrum said...

The studies shown in The Battle of the Diets: Is Anyone Winning (At Losing?) at 40:55, 41:19, 42:19 and 42:53 indicate that insulin-sensitive people lose more weight than insulin-resistant people on low-fat, high-carb/GL diets.

Confused? I certainly am.

Melchior Meijer said...

I have never understood the idea that overweight people would be more insulin resistant (less insulin sensitive) than lean people. If anything, you would expect that insulin sensitive people would store fat easier than insulin resistant people.

Yet almost everybody in the low carb world claims that their overweight clients are fat 'due to insulin resistace'. Well if they are so insulin resistant, how could they have gained the weight. My understanding of this is a mess...

CarbSane said...

Certainly confusing what to make of all of it. I do think folks who are IR seem to do better on LC (at least initially). This may be because their glucose metabolism is messed up so a low fat CRD is not satisfying thus difficult to stick with. But ketones & fatty acids make their way into cells just fine and appetite is reduced. I know in my case, early into LC, I probably went some days on like 500 cal/day WITHOUT doing so deliberately, but if you gave me a standard women's LF CRD of 1200 cal/day I doubt I would have been able to follow it for very long.

What I guess this all boils down to is finding a WOE that works best with one's metabolism to achieve a caloric deficit for sufficient time to lose weight (fat).

Nigel Kinbrum said...

Fat cells can store fatty acids when serum insulin level is low. People with insulin resistance have chronically high serum insulin level.

My theory why insulin resistance makes it easy to gain weight/difficult to lose weight on high-carb/GL diets is as follows:-

Insulin resistance -> chronic hyperinsulinaemia -> impaired/no phase 1 insulin response -> increased variation in blood glucose level after eating high-GL carbs -> increased hunger as blood glucose level falls -> over-eating -> excessive intake of calories.

CarbSane said...

Melchior, this is because too many in low carb circles have the whole insulin/IR thing backwards. It is obesity (overstuffed fat cells) that leads to the resistance to insulin and chronic hyperinsulinemia. Small fat cells are insulin sensitive, large ones lose their sensitivity. Insulin resistance arises when the body can no longer store excess fatty acids where they belong - in the fat cells - circulating levels rise, lipid and metabolites accumulate in tissues causing dysfunction, etc. There are lean IR folks, they simply exceed the limits of their fat stores.

It is not postprandial insulin levels that drive fat accumulation no matter how many times it's repeated. It is chronic positive caloric balance.

I also believe we need to distinguish between acute IR and chronic. It has been shown that a single high fat meal can induce an IR state in terms of impaired glucose clearance. But this eventually reverses and I'm not sure how much this alters insulin levels. Chronic IR is due to free fatty acid release. Those FFA's can act directly on the pancreas to stimulate insulin production - voila! Chronic hyperinsulinemia. So dietary fat doesn't stimulate a postprandial insulin response, but when we can't keep it in proper storage, the fatty acids can stimulate basal insulin levels to rise.

CarbSane said...

Methinks you got it Nige! On LC this is all short-circuited. Fatty acid levels are regulated by release from fat stores, not dietary levels. Blood glucose levels will be more stable, even if still elevated, when they are controlled solely (or mostly) by gluconeogenesis with no dietary contribution.

It does appear, however, that after a period of time, this wears off considerably.

malpaz said...

im confused... do you want a postprandial insulin response from a fatty meal? you said it doesnt stimulate one? does that mean your glucose rises but the pancreas doesnt secrete insulin?

what do you mean by 'keep it in proper storage'?

i get what nigel says but he just starts with IR...its gotta be caused by something or come from somewhere

CarbSane said...

Hi Mal, I actually have a post in the hopper about this that I think I'll dust off and finish up as regards fatty acids and insulin and why our bodies regulate the free fatty acid levels the way they do. But by "proper storage" I refer to the fact that fats are intended to be stored in our fat cells with only limited amounts in other tissues (ectopic storage). It is when we exceed our ability to store it where it is supposed to be that too much lipid infiltrates our ectopic tissues and exerts toxic effects. Chronic IR (as opposed to transient resistance due to a large fat meal)is caused by caloric excesses to where we have reached the limits of our fat stores. This is highly individual and it appears that those with more subQ fat have a higher threshold because they have more safe places to store the excesses. One thing I'm almost certain of: using insulin is not the cause of resistance to its action.

James said...

Exercise, in and of itself, is a hard way to lose weight. Doesn't work for most simply because it's far easier to down an 800-calories Big Mac than burn those calories off. So to be effective, it needs to be combined with diet, which I think goes right along with what Gary's saying. Or just take Phentemrine...

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