Cardiovascular disease

#247: Why LDL-Cholesterol (Bad) Shifts On a Ketogenic Diet and Inflammation w/ Dave Feldman

by Mike Mutzel

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About Dave Feldman

Dave’s a senior software engineer and entrepreneur who began a low-carb, high-fat diet in April 2015 and have since learned everything he could about it with special emphasis on cholesterol; given that his lipid numbers spiked substantially after going on a metagenic diet.

As an engineer, Dave spotted a pattern in the lipid system that’s very similar to distributed objects in networks.

Through research and self-experimentation he’s revealed some very powerful data about how cholesterol fluctuates with energy intake. He can reliably and shift his cholesterol numbers around by over 100 points (mg/dL) in days by just shifting his energy intake.

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MonoSorb 1300 | 600 mg EPA | 260 mg DHA | Monoglyceride Fish Oil | IFOS Certified | Enteric Coated

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twitter.com/DaveKeto

https://cholesterolcode.com/about/

Patreon.com/DaveFeldman

 

Show Notes

 

04:18 Dave received scary cholesterol results. His total cholesterol was 329. He scheduled a second test for two weeks later. During that time, he learned all he could about cholesterol. A pattern emerged. It was a combination of depression and fascination in the lipid pattern. On his second test, his LDL and total (now 424) had jumped up substantially. His depression caused him to drop his caloric intake. He stayed keto, though his intake of saturated fat dropped. He lost weight. He was certain that his numbers would go down because he ate little fat.

06:22 Analogy: Your body makes boats that ship things that are hydrophobic, doesn’t like to swim in blood. Fat is hydrophobic.

06:58 If fatty acids come from ingested food, the boat is chylomicron. This is cleared right away. When the cargo comes from adipocytes, it is packaged in your liver as VLDLs that are remodeled to become LDLs. The cargo in VLDLs are fatty acids and cholesterol, which becomes LDL. This explains why fat burners have higher LDL.

08:34 More boats. Because Dave brought down his caloric load during the two weeks, meant less incoming fat, fewer chylomicrons and more mobilization of fatty acids from adipocytes into the liver, thus making more VLDLs and more remodeled LDLs and more LDL cholesterol.

09:33 Triglycerides are not dumped. They are being provided to your tissues as a form of energy. The remodeled LDL particle: Did it start as a VLDL? Did it deliver its cargo of energy? Is it adrift in the vascular system unused?

10:37 There are studies that show that high LDL levels in people who are low carb/high fat is not carcinogenic. When you become powered by fat, your total and LDL cholesterol could go up. Our current medical belief is that high LDL means you are going to die.

15:15 Persistent insulin in the body causes atherogenic dyslipidemia. Low HDL with high triglycerides with small dense LDL particles.

15:39 Dave sees small dense LDL particles as smaller boats. He would like more lipid data sets that include fasting insulin.

16:37 Triglycerides can become elevated with immune and inflammatory responses that ramp up VLDL levels.

17:11 Part of a lipoprotein’s role is to bind to pathogens, as well as provide a means of coverage for antioxidants like alpha tocopherol, a form of vitamin E.

18:33 In an experiment, when adding HIIT and then weight lifting, Dave found that his LDL dropped by 11% and then 13%. His theory is receptor-mediated endocytosis in peripheral muscle tissue, where muscle tissue grabs LDL particles for repair.

21:11 LDL vehicles can have a number of different jobs. An Apo B protein from the liver delivers triglycerides, then takes a support role for 2 to 4 days. Perhaps this is so they can bind to pathogens or take a reparative role.

23:37 High triglycerides are a powerful leading indicator of a problem if it is not being dropped off and used as an energy source.

23:49 Being past your personal fat threshold elevates triglycerides, where they are stored in adipose tissue and other organs. This process, however, keeps the triglycerides out of the blood stream.

26:45 Free radicals running loose are like anti-matter of our bloodstream. It can ultimately trigger a chain oxidation.

28:15 Ancestrally, people with hypercholesterolemia have the same or better survival rate. .

31:41 HDL cholesterol rises with fat burning adaptation. If you are secreting higher VLDLs, you are bringing up more HDL.

32:20 HDL is not well understood. HDL function includes and immune responses.

34:30 Statin data is tightly controlled and only positive data is released. Statin drugs have only been studied for risk cardiovascular events, but not the other impacts of lowering LDL.

42:54 Tribalism prevails in medical science. It is an obstacle. Dave’s data has not been welcomed or embraced.

45:47 Lean Mass Hyper-Responders may be a superior metabolic profile. They tend to have LDL above 200, an HDL above 80 and triglycerides of 70 or lower. They often say that it is the best that they have ever felt.

49:00 The Lipid Energy model is that VLDL will create LDL at rates dependent upon demand/need.

50:22 Lean Mass Hyper-Responders with the highest levels of LDL tend to be very lean and very active. Carotid intima media thickness imaging on an ultra-marathoner Lean Mass Hyper-Responder with whom Dave works, shows results of someone much younger.

52:53 Part of high LDL in Lean Mass Hyper-Responders could be autophagy-driven cellular renewal, since they have enormous potential for autophagy as fat burners.

54:00 Lean Mass Hyper-Responders have challenges fasting for long periods of time, because, in a sense, they already are, from their body’s perspective.

56:44 Remnant lipoproteins are atherogenic.  Remnants that can be detected are VLDLs. If you are past your personal fat threshold/hyperinsulinemic, your body will have problems processing its existing lipid energy metabolism. That is associated with higher levels of cardiovascular disease.

01:00:00 As long as your HDL is reasonably high and triglycerides are low, one need not be concerned about the cardiovascular risk of elevated LDL.

01:03:15 It is no longer required to fast before lipid testing. This skews test results. If you are low carb, having eaten a fatty meal. The triglycerides from the meal will be end up in your bloodstream for hours.

01:04:44 Triglycerides should not be elevated in a fasted test. If they were elevated, as a low carb person, you may not be utilizing your existing fat stores.

01:05:21 Remnant cholesterol studies are being done on non-fasted tests. People on a low carb diet have lower basal insulin and bolus insulin and will have relatively longer resonance time of fat in chylomicrons and VLDL.

01:10:31 Dave sees cholesterol tests as a diagnostic tool. Illness can impact many different markers, like ferritin and lipids, including LDL.

01:15:46 Dave seeks support for his work on Patreon.com/DaveFeldman.

01:16:58 Dave’s elevator pitch is that the way science is done needs to change. We need transparency, improved peer review, and increased publically archived data.

 

Related Podcast: #179: Jeffry Gerber, MD- Insulin Resistance Not Cholesterol Causes Heart Disease

 

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