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  #1   ^
Old Wed, Mar-31-21, 15:10
GRB5111's Avatar
GRB5111 GRB5111 is offline
Posts: 3,645
Plan: Very LC, Higher Protein
Stats: 227/186/185 Male 6' 0"
Progress: 98%
Location: Herndon, VA
Default Recent Meta-Analysis Finding: Insulin Resistance Precedes Obesity

For those who believe that obesity causes diabetes rather than consuming too many unhealthy and/or processed foods:

"Conclusions and Relevance In this meta-analysis, the finding of temporal sequencing (in which changes in fasting insulin level precede changes in weight) is not consistent with the assertion that obesity causes noncommunicable chronic diseases and premature death by increasing levels of fasting insulin."

Fasting Insulin and CRP

There were 42 pairs of standardized slopes from 27 cohorts and 16 studies that measured both fasting insulin and CRP levels (Table 2). Most fasting insulin and CRP standardized slopes were negative (74% of fasting insulin slopes and 63% of CRP slopes), suggesting that participants in most studies experienced decreases in insulin and CRP levels. The association between period 1 CRP level and period 2 fasting insulin level was not significant (β = 0.19; 95% CI, 0.04 to 0.42; I2 = 49%). The association between period 1 fasting insulin level and period 2 CRP level was positive and significant (β = 0.29; 95% CI, 0.10-0.47; I2 = 36%), suggesting that for every unit of SD change in period 1 insulin level, there was an associated change of 0.29 units of SD in period 2 CRP level. There was moderate heterogeneity. The subgroups did not significantly modify the associations between fasting insulin and CRP levels (eTables 2 and 3 in the Supplement)."

Insulin resistance, a cause and consequence of hyperinsulinemia,89 leads to type 2 diabetes and is associated with other adverse outcomes, such as myocardial infarction, chronic pulmonary disease, and some cancers,90,91 and may also be indicated in diabetic nephropathy.92 Despite the 3 scenarios described earlier, it is commonly believed that obesity leads to hyperinsulinemia.93-95 If the converse is true and hyperinsulinemia actually leads to obesity and its putative adverse consequences, then weight loss without concomitant decreases in insulin (eg, liposuction) would not be expected to address these adverse consequences. In addition, weight loss would not address risk in people with so-called metabolically healthy obesity, that is, those without insulin resistance.

Of interest, insulin resistance is also present in lean individuals, in particular men and individuals of Asian descent.97 These 2 groups are at heightened risk for type 2 diabetes98 and cardiovascular disease, yet are more likely to be lean than women and individuals not of Asian descent. These observations are consistent with the hypothesis that hyperinsulinemia rather than obesity is driving adverse outcomes in this population. We speculate that the capacity to store the byproducts of excess glucose by increasing the size of fat cells (manifested as obesity) might delay the onset of type 2 diabetes and its consequences in some individuals, thus explaining the so-called obesity paradox of lower mortality among people with obesity. This idea, although not new,99 fits better with the emerging evidence. If this speculation is correct, assessing the capacity to store such by-products at the individual level may be a useful step toward personalized medicine.

Although it is possible that hyperinsulinemia per se is not the causal agent that leads to adverse outcomes (but is rather a marker for another more proximate factor), this would not change the lack of support for recommending weight loss among people with obesity. Rather, other markers should be investigated that, although correlated with obesity, are more strongly associated with premature mortality because they also exist in lean individuals. Therapies that lower insulin levels (eg, moderate diets with fewer simple carbohydrates and metformin) may be sustainable if an intermediate marker other than weight is targeted. Because the prevalence of obesity continues to increase worldwide, additional studies to confirm this hypothesis are urgently needed, not least because public health campaigns promoting weight loss are ineffective and lead to stigma among those with obesity.

I highlighted this statement in bold: "If this speculation is correct, assessing the capacity to store such by-products at the individual level may be a useful step toward personalized medicine." Where have I heard this before . . . ?

Study Report:

Last edited by GRB5111 : Thu, Apr-01-21 at 12:28.
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  #2   ^
Old Thu, Apr-01-21, 07:53
WereBear's Avatar
WereBear WereBear is offline
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Posts: 13,283
Plan: Epi-Paleo/IF
Stats: 220/123/150 Female 67
Progress: 139%
Location: USA

To think otherwise is to fall for the also debunked: "just eat less and move more" fallacy.
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  #3   ^
Old Thu, Apr-01-21, 15:53
Zei Zei is offline
Senior Member
Posts: 1,582
Plan: Carb reduction in general
Stats: 230/185/180 Female 5 ft 9 in
Progress: 90%
Location: Texas

Originally Posted by WereBear
To think otherwise is to fall for the also debunked: "just eat less and move more" fallacy.

Definitely agree. Incorrect belief that obesity precedes and causes disease invites blaming the patient for gluttony/sloth/poor personal choices.
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  #4   ^
Old Thu, Apr-01-21, 16:07
Ms Arielle's Avatar
Ms Arielle Ms Arielle is offline
Senior Member
Posts: 15,366
Plan: atkins
Stats: 255/232/200 Female 5'8"
Progress: 42%
Location: Massachusetts

Which comes first, the cart or the horse?

Frustrating that we are no closer to mainstream support and understanding of the problem. Obesity is caused by food choices. And too much food.

Talk ed to a nurse yesterday who dropped #100. Boy, she looked great. Gastric bypass. Our kids went to school together
We reminisced over all the cupcakes that the parents delivered to grammar school to feed a whole classroom to celebrate their child's birthday. Just junk food.

She mentioned that cupcakes are common at her place of work.....
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