Elevated Visceral Fat: "Nobody Wants That"

The language that follows is the language of observational/epidemiological studies:

"among obese adults, visceral fat was associated with more than a twofold increased risk of developing incident diabetes (odds ratio 2.42, 95% CI 1.59 to 3.68).  In addition, developing either condition was also associated with markers of insulin resistance including elevated fructosamine levels (OR 1.95, 95% CI 1.43 to 2.67) and elevated fasting blood glucose (OR 1.88, 95% CI 1.38 to 2.56).

But there were no associations with general markers of obesity, including body mass index (BMI) or total body fat."

In other words, "these are interesting correlations."

Not that I would disagree with their conclusions:

"Our study may have implications for understanding differences between metabolically healthy and pathologic obesity."

This is interesting because not everyone that's fat is insulin resistant, and those who are develop illness as much higher rates than those who are not.

This is also interesting:

"In participants without diabetes at baseline, a number of factors were significantly and independently associated with incident diabetes in obese adults:

• Elevated visceral fat: OR 2.42, 95% CI 1.59 to 3.68 (P<0 .001=".001" li="li">
• Elevated systolic blood pressure: OR 1.26, 95% CI 1.07 to 1.48 (P=0.006)
• Elevated fructosamine levels: OR 1.95, 95% CI 1.43 to 2.67 (P<0 .001=".001" li="li">
• Elevated fasting blood glucose: OR 1.88, 95% CI 1.38 to 2.56 (P<0 .001=".001" li="li">
• Weight gain from baseline: OR 1.06, 95% CI 1.02 to 1.10 (P=0.002)
• Family history of diabetes: OR 2.32, 95% CI 1.25 to 4.29 (P=0.008)

"There were no associations for BMI, total body fat, or abdominal subcutaneous fat, they reported." 

Many of the same factors correlated with the development of insulin resistant in those not obese when the study began.

http://www.diabetesincontrol.com/index.phpoption=com_content&view=article&id=13578&cacatid=1&Itemid=17

All in all, this fits a well recognized pattern of illness - high fructosamine levels/high fructose intake, visceral fat, high blood pressure, elevated fasting glucose, weight gain, and family history of diabetes.  

Lucky for us, most of these symptoms are treatable through carb restriction - I recommend starting out at 25-50g/day to stop these symptoms, and after weight/fat/symptom normalization, many will be able to eat more carbs but maintain their wellness.  Eat meat, eggs, vegetables, nuts and seeds, little fruit or starch, no sugar/wheat.

Indicators For Insulin Resistance

Abstract

BACKGROUND/OBJECTIVES:

 

Lipid accumulation product (LAP) is an index, which combines waist circumference (WC) and triglyceride (TG) reflecting lipid accumulation. The aims of the study were to explore the relationship between LAP and insulin resistance (IR) and to assess whether LAP was superior to WC and body mass index (BMI) in identifying IR.

SUBJECTS/METHODS:

 

The study was cross-sectional and included 2524 non-diabetic subjects from China. The blood pressure (BP), anthropometric measurements, glucose levels, insulin levels and a fasting lipid profile were measured. BMI, the homeostasis model assessment of IR (HOMA-IR) and LAP were calculated.

RESULTS:

 

In both sexes, BP, BMI, total cholesterol (TC), non high-density lipoprotein cholesterol (non-HDL-C), HOMA-IR, fasting and postprandial glucose levels increased across LAP quartiles (P<0 .001=".001" across="across" cholesterol="cholesterol" decreased="decreased" hdl="hdl" i="i" lap="lap" levels="levels" quartiles="quartiles" while="while">P

<0 .001=".001" analysis="analysis" and="and" bmi="bmi" both="both" correlated="correlated" correlation="correlation" demonstrated="demonstrated" hdl-c="hdl-c" homa-ir="homa-ir" i="i" in="in" lap="lap" non-hdl-c="non-hdl-c" pearson="pearson" s="s" sexes="sexes" tg="tg" that="that" was="was" wc="wc" with="with">P<0 .001=".001" a="a" analysis="analysis" and="and" bmi="bmi" demonstrated="demonstrated" greater="greater" had="had" homa-ir="homa-ir" impact="impact" lap="lap" multivariate="multivariate" on="on" p="p" than="than" that="that" wc.="wc.">

CONCLUSIONS:

 

LAP is closely associated with HOMA-IR and is a powerful index that outperforms BMI and WC in identifying IR in non-diabetic individuals.

http://www.nature.com/ejcn/journal/v66/n9/abs/ejcn201283a.html?WT.ec_id=EJCN-201209

The BLUF:  BMI based measures do not indicate poor health (as measured by insulin resistance) as well as an index of waist circumference and triglyceride levels.   And why wouldn't it?  Waist circumference changes and decreasing triglycerides are hall marks of carb restrictions.

Eades: Leptin Basics

The venerable Dr. Mike Eades does a nice job explaining about leptin and hunger, and how carb restriction affects these things - more powerfully than drugs.

The drug rimonabant (Acomplia) that failed to pass muster with the FDA panel last week works by blocking some of the hunger receptors in the brain. In other words, those who take the drug – assuming it works as touted – will be less hungry. Less hunger means less food consumption. Less food consumption typically results in weight loss. So, if you take rimonabant, assuming you don’t become suicidal and do yourself in (the big worry of the FDA panel since the major side effects are varying degrees of psychoses), you should lose some weight. But there is a better, cheaper way.

The low-carbohydrate diet working through the hormone leptin reduces hunger much more than rimonabant on its best day. And without the risk of serious side effects. And without the $250 per month for the drug.

http://www.proteinpower.com/drmike/metabolism/leptin-low-carb-and-hunger/

The summary:

1.  Fat makes leptin, so as fat decreases leptin decreases, signaling the brain to make the human hungry.  This way, the human cannot run out of fuel - unless the hunger is not sufficiently motivating (it usually is - funny what millions of years of evolution will do for you) to get the human out to hunt/gather; or, there's inadequate amounts of stuff to be hunted/gathered.

2.  Obese folks have mucho leptin - much more than normal, but their body does not translate the leptin into decreased hunger.  

3. The reason the obese are not leptin sensitive starts with triglycerides - when trigs are high, leptin does not cross the blood brain barrier (BBB), so for practical purposes, the leptin does not exist.  

4.  Carbohydrate restriction helps restore this process by reducing triglyceride levels, which allows leptin to cross the BBB, and restore leptin sensitivity.

Fructose also seems to have a negative effect on leptin sensitivity.

Once again, it's the neolithic levels of carb intake, exacerbated by high neolithic-fructose intake, which drives the system off its energy management program, resulting in humans feeling hungry when they are not in need of more food.

Minor edits 27 July 2012