Article from the Heart Scan Blog - of Wr William Davis
Low carb - but triglycerides go. . . up?"
“How could that happen? You said losing weight would make my HDL go up and my triglycerides go down!”
Yes, I had said that. But I was oversimplifying.
The truth is that, when there is weight loss, especially profound weight loss like Brad experienced eliminating wheat and cornstarch products, there is mobilization of fat stores. Fat is stored energy. Energy is stored as . . . triglycerides.
So when there is substantial weight loss, there is a flood of triglycerides in the blood, and triglyceride levels in the midst of weight loss can commonly jump up, not uncommonly to the 200-300+ mg/dl range. When triglycerides go up, there is also a drop in HDL (triglycerides interact with HDL particles, modify their structure and make them more readily destroyed, thereby dropping blood levels). Occasionally, substantial weight loss like Brad experienced will drop HDL really low, as low as the 20′s.
Once weight stabilizes, this effect can last up to 2 months before correcting. Only then will triglycerides drop and HDL rise. The rise in HDL occurs even more slowly, requiring several more months to plateau.
In other words, weight loss like Brad’s causes triglycerides to increase and HDL to decrease, to be followed later by a drop in triglycerides and a rise in HDL.
I know of no way to block this phenomenon.
And perhaps we shouldn’t, since this is how fat stores are mobilized and “burned off.”
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August 16, 2008 at 1:33 am
- Hi Dr Davis,While fat is stored as triglycerides, it is released from adipose stores as non esterified fatty acids, and these will be predominantly palmitic acid in humans. Non esterified palmitic acid appears to be an excellent inducer of insulin resistance, and insulin resistance has been hypothesised by several authors to be a completely normal physiological adaption to fasting or seasonal carbohydrate absence. While weight loss is on going, the circulation is flooded with NEFA and “physiological” insulin resistance should predominate. If the person continues to consume “good” carbohydrate at above acute metabolic needs, the excess will get shipped out of the liver as VLDLs. Under insulin resistance lipoprotein lipase, routinely under the control of insulin, won’t be doing much lipolysis and so VLDLs can hang around in the circulation… Muscle can happily accept NEFA as a prime source of energy without lipoprotein lipase having to split the lipids from VLDLs, so leave the VLDLs there to show up as fasting trigs….Once weight is stable the NEFA release from adipose tissue will be much better matched to metabolic needs. With the improved insulin sensitivity due to loss of visceral fat, control of both adipose hormone sensitive lipase and endothelial lipoprotein lipase activity should normalise and allow VLDLs and HDL to settle in to more cardiologically acceptable numbers.Just an idea. The prediction it makes is for a reduced HbA1c due to the reduction in bulk carbohydrate (this must happen to allow lipolysis for weight loss), coupled with no drop or an increase in fasting blood glucose due to the NEFA induced insulin resistance. Very curious as to whether this happened…Idea is open for kicking.Peter
