Eat more carbs and less fat to produce NAD+ and generate energy
One of the key take-homes from this is that if you want to be optimally healthy, you want to burn glucose in your electron transport chain of your mitochondria, and one of the best ways to ensure that is to increase carbs and lower your fat intake.
As explained by Marshall, when you eat a meal, insulin is released. When you consume a meal that generates a lot of insulin, it suppresses the release of free fatty acids from your fat cells. Those free fatty acids are what cells import and burn in the mitochondria.
“Essentially, what the insulin is doing is it’s kind of telling the fat to get out of the way because you can’t efficiently burn fat and glucose at the same time because of the Randle cycle. The burning of fat will displace your ability to burn glucose,” Marshall explains.
“So, insulin lowers the amount of fat that can enter the mitochondria. Interestingly, it also lowers the amount of branched-chain amino acids that are circulating.”
Marshall struggled with elevated blood glucose in the mornings and, as an experiment, he swapped muscle meat and protein from grains for bone broth and pork rinds.
“Papers have shown there’s this competition between branched-chain amino acids that are high in muscle meats and grains, and glycine that is high in connective tissues, collagen, gelatin,” he says.
Within about two weeks, his fasting blood glucose was reliably right around 80, which is optimal. He was consuming about 600 grams of mostly starch and some sugars, primarily sucrose from whole fruit.
The problem with pure fructose, such as agave nectar, is it doesn’t activa
activate insulin, and without the insulin signaling, your body won’t be able to burn that fructose. So don’t eat agave nectar. Sucrose, however, does generate an insulin response, as does starch.
Fat Burns in the Flame of Carbohydrate
As noted by Marshall, many traditional cultures eat high-starch diets and have very high metabolic rates. That’s an important point. If your metabolic rate is low and you’re eating plenty of healthy carbs, it could be that your fruit intake is too high and you need more starchy foods.
“When you eat a lot of starch and glucose, and you look at what happens in the mitochondria when you’re burning the glucose efficiently, it lowers NADH. You get high NAD+ and low NADH when you are actively burning glucose,” Marshall says.
“I think the reason for that probably has to do with what I said before. The pyruvate dehydrogenase generates ROS, and NNT replaces the NAD+. But it doesn’t really matter why. The point is, if you’re actively burning glucose, you’ll have high NAD+ availability, and that’s what you need to run your metabolism. Those electrons need to go somewhere, and they want to go to NAD+ …
There is an old saying in the medical literature: Fat burns in the flame of carbohydrate. You can find this in the 1920s, 1930s if you search PubMed. I think the reason for that is that when you’re burning carbohydrates, you’re increasing the amount of NAD+, and fat requires a lot of NAD+ to burn.
Fat requires a lot of oxygen to burn basically, and NAD+ is essentially playing the role of oxygen in the mitochondria. It’s oxidizing the fat. And so, I think burning carbohydrates generates enough NAD+ that you can burn fat more efficiently and more cleanly.”
How Elevated NADH Affects Your Fat Composition
Elevated NADH also affects your fat composition. There’s an enzyme called SCD1 that converts saturated fat in your body to monounsaturated fat, and that enzymatic reaction uses NADH. So, if you are in reductive stress, which means you have elevated NADH, you’re going to convert a lot of your saturated fat into monounsaturated fat. Again, that’s because you have surplus electrons that are looking for a home and they find this home on that enzyme.
Monosaturated fat is soft, while saturated fat is firm. And, recall the discussion about pig fat, the way to make it firmer is by increasing starch. If you have mostly saturated fat in your body, you’re going to have high NAD+ availability and a fast metabolic rate.
Why High LA Is Associated With Decreased Diabetes Risk
Paradoxically, reputable researchers have shown that high LA levels are associated with a decreased risk of diabetes. Biologically, this made little sense to me, considering LA is the most significant metabolic toxin in your diet, until Marshall explained it.
When you’re in reductive stress and you high NADH, the activity of desaturase enzymes increases. SCD1 converts stearic acid to oleic acid. But another one called delta-6 desaturase or D6D puts a third double bond into LA (which has two double bonds), and that’s the limiting step in LA’s conversion to arachidonic acid.
Arachidonic acid gets built into cell membranes, and once it’s released, it can oxidize. So, when you’re in reductive stress, you start converting LA to arachidonic acid that then becomes oxidized 5-HETE, 12-HETE and 15-HETE, which are associated with disease, including cardiovascular disease.
“The 5-HETE, 12-HETE and 15-HETE feed back and activate PPAR-α and aryl hydrocarbon receptor, and they in turn increase the amount of these desaturase enzymes that we’re making,” he says.
“So, you have this huge feedback loop where the polyunsaturated fat is getting oxidized, and that is a signal to convert more of your saturated fat into monounsaturated fat. So, the pattern that predicts diabetes, heart disease, obesity is low saturated fat, especially low stearic acid, low linoleic acid, because that’s all getting oxidized.
If you have high monounsaturated fat and low polyunsaturated fat, that’s actually a really bad sign. That doesn’t mean that you should run out and start swilling soybean oil because the polyunsaturated fat is part of the system that is creating the problem.
It’s just that it burned as part of the process. It’s not the thing that accumulates really. And in fact, it’s sort of the opposite. There are breeds of pigs that we’ve selected to remain very lean, and if you take one of these hogs and feed them sunflower oil or sunflower seeds … the lard was something like 54% linoleic acid. So, these lean breeds of hogs just accumulate the linoleic acid, they don’t oxidize it.
Whereas if you look at a fatty breed of hog like a Mangalitza, when you feed them linoleic acid or other vegetable oils, they convert all that linoleic acid to monounsaturated fat and they remain much lower. That’s the difference between the hog that remains metabolically healthy and the hog that becomes obese and probably insulin resistant — the metabolically healthy hog isn’t oxidizing the linoleic acid.
And of course, one of the main reasons why that hog would oxidize the linoleic acid is that it’s in reductive stress, because the reductive stress drives the desaturation of those fats in the first place. It drives the activity of delta 6 desaturase, and that’s really the key gating step that is predictive in humans of diabetes and results in that pattern of low stearic acid, high oleic acid, and low linoleic acid.”
While high LA is associated with decreased diabetes, if this process continues, problems will eventually occur.
Measuring Your Redox Balance
In the interview, Marshall explains how we intend to measure the cellular redox balance of patients by testing redox pairs like pyruvate and lactate, which reflect the redox of the cytoplasm, and acetoacetate and beta-hydroxybutyrate, which reflect the redox of the mitochondria. Why is this important? Marshall explains:
“In the mitochondria, you want to have high NAD+ because that’s where your metabolism is happening. That is going to tell you how fast your metabolic rate’s going to go, et cetera. Whereas in the cytoplasm, that’s where desaturase reactions are taking place and lactate is being produced.
If you have high NADH in the cytoplasm, that’s when you start oxidizing your linoleic acid, that’s when you start converting stearic acid to oleic acid and that’s when you start creating the 5-HETE and the 12-HETE.
So, you want to know what’s happening in both places, and it’s complicated. There’s interplay back and forth between both of them and if the mitochondria are overwhelmed and spitting out tons of reactive oxygen species, then the cytoplasm can also get oxidized. So, you really want to know both.”
Also, when you have high NADH in your cytoplasm, you’re going to activate the SCD1 enzyme that reduces LA. It lowers it, which superficially feels like a good thing, but it’s not, because it’s taking the LA out of your fat stores, causing it to oxidize, and it’s the oxidized metabolic byproducts, the breakdown products, that cause the most damage.
Ideally, you want to excrete LA very slowly. Provided you have good liver function, it will attach to glucose and be excreted in your urine without getting oxidized. This is a slow process, so you must be patient. If the LA is released to rapidly, you’ll end up with severe damage that will raise your risk for chronic diseases such as cancer and heart disease.
More Information
To learn more, please listen to the interview in its entirety. You may need to listen to it several times, even, to really understand it. Once you do, however, the answers to many of your health problems will become that much clearer.
In the interview, we also discuss the potential problems of branched-chain protein (red meat) and the benefits of collagen or gelatin, which are high in the amino acids glycine, proline and hydroxyproline. Importantly, glycine helps to directly eliminate reductive stress.
We also review the benefits of stearoylethanolamide (SEA) supplementation. SEA is a natural compound your body makes from stearic acid in your adipose tissues. So, your blood level of SEA is reflective of the stearic acid levels of your adipose tissues. As you progress towards metabolic syndrome, diabetes, obesity and heart disease, your stearic acid levels drop.
Ideally, your SEA level should be around 8%. The average now is only around 3% to 3.5%, which helps explain why about 95% of Americans are metabolically inflexible. SEA also helps regulate your cannabinoid system.
If you want to dive deeper into molecular biology, be sure to check out Marshall’s YouTube channel, Fire in a Bottle.
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Source: https://tapnewswire.com/2024/04/eat-more-carbs-and-less-fat-to-produce-nad/
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