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About Ben Bikman, PhD
The focus of Ben's lab (the Laboratory of Obesity and Metabolism) is twofold. First, we aim to identify the molecular mechanisms that explain the increased risk of disease that accompanies weight gain, with particular emphasis on the etiology of insulin resistance and disrupted mitochondrial function. Second, we hope to reveal novel cellular processes that are responsible for fat development.
Connect with Ben
05:49 We are applying the low carb ketogenic diet in bizarre ways by dumping oil into their drinks. There is no other nutritional value to the oils. Eggs are loaded with nutrition. Dr. Bikman mixes raw egg into his morning tea.
07:45 Fasted exercise stimulates glucagon. Our red blood cells need glucose. When we need gluconeogenesis, glucagon will be elevated. If you are low carb, exercising in a fasted state, or you are fasted, you need gluconeogenesis. Glucagon will be elevated and insulin, which inhibits gluconeogenesis, will be low.
09:37 People may be confusing gluconeogenesis with an insulinogenic effect. If you are low carb, gluconeogenesis happens only as much as you need it.
10:40 If you have ketogenesis happening, you have gluconeogenesis. Fat is used for fuel, and parallel, we have the need for new essential glucose to be produced.
13:14 Depleting glycogen is a necessary event before ketogenesis kicks in.
14:10 True clinical hypoglycemia is remarkably uncommon. If you are insulin resistant, and your brain has been depending upon high glucose and has had no time to adapt to using ketones for fuel, glucose levels can get low. Your body senses this and panics. There is more than enough glucose.
17:03 There are two phases of hunger. The first phase is hunger from empty guts. It is passing. The second phase of hunger is when your body says that there is a genuine deficiency of energy and you want to eat anything and will do anything to get it.
18:22 As long as you have sufficient salt and water consumption, you are good for exercise. If you have food in your gut, your body is conflicted about sending blood to your muscles or your guts.
19:57 Protein increases insulin and glucagon. Other macros increase one or the other.
21:02 Glucagon is catabolic of fat tissue. There are not many glucagon receptors in muscle.
21:55 If you are low carb or fasted and you need gluconeogenesis, there is no appreciable increase in insulin from the protein, yet a substantial increase in glucagon.
23:00 Glucagon activates lipolysis, increasing free fatty acids. The liver sees more fatty acids, but since insulin is low, the liver will not store the fat. Hormones tell the body what to do with energy.
23:54 Acetyl-CoA is the branch point of all metabolic processes in the liver and most other cells. It can be used for creating new glucose, activating gluconeogenesis, create lipids through lipogenesis and it can to into the citrate cycle and be used for energy, creating ATP, or it can be used for ketogenesis. All of this is dependent upon insulin. Catecholamines and glucagon counter insulin, but insulin reigns supreme.
25:40 Consuming meat or saturated fat does not create lipotoxicity, nor insulin resistance.
27:36 In animal and human studies of saturated fat, fat was administered intravenously. Elsewhere it was tested against muscle tissue in the lab, which does not reflect the complex systems of the body, especially the influence of insulin. Both of these formats helped to form our mechanistic thinking of how saturated fat can cause insulin resistance.
30:17 It is easier to induce insulin mediated lipotoxicity with a vegan diet than a ketogenic diet due to the high carb content.
30:43 Excess palmitate can create an excess of ceramides, as can hyperinsulinemia directly.
32:39 Triglycerides do not effect insulin sensitivity.
33:45 There are more ceramides in sedentary, obese, insulinemic individuals. They also have higher levels of circulating fatty acids. This is because the liver is making more fat or the adipocytes are becoming increasingly insulin resistant. Thus adipocytes are spilling lipid into the blood. The lipids switch from inert triglycerides to ceramides.
34:53 Alpha cells become insulin resistant because of a ceramide accumulation. We have a microenvironment in the pancreas. Butted up against each other, you have an alpha cell that releases glucagon and a beta cell that releases insulin. Insulin from the beta cell tells the alpha cell not to make glucagon. Within this environment is a greater amount of insulin than in our system. This means that the alpha cell is getting hundreds, maybe thousands of times more insulin than other tissues.
35:52 In type 1 diabetes, where you are not making insulin in the microenvironment, too much glucagon is produced, elevating glucose.
36:18 An insulin resistant person, who’s insulin levels have been climbing over the decades, but there is enough to keep glucose in check, remains clinically silent. Viewing diabetes as an insulin disease results in better treatment and earlier detection.
36:43 Eventually, glucose levels rise and you are a type 2 diabetic. This could be when the alpha cells become insulin resistant. Insulin tells the alpha cell to make less glucagon, unless the alpha cell becomes insulin resistant and glucagon climbs. This signals the liver to start pumping out glucose.
37:30 Both insulin and glucagon are high in type 2 diabetics. It should be one or the other.
38:13 Weight gain results from insulin therapy for both type 1 and type 2 diabetics, even if caloric consumption remains the same.
40:15 Exogenous ketones shut down your body’s ability for hepatic ketogenesis. Pulsed exogenous ketones can be helpful with TBI or other neurological issues.
41:55 Glucagon activates processes that are involved in mitochondrial biogenesis.
44:18 Ketones are energy. When you do endurance exercise with high blood glucose, glucose drops. When you do endurance exercise in a fat adapted state, your ketones will drop.
44:47 As you become more fat adapted, your body becomes more efficient and ketone baseline levels drop.
44:57 The definition of ketosis had been arbitrarily set at .5 mml. It is being considered to start at .3 mml due to the body’s efficiency shifts in fat adaptation. Once ketones are detectible from a low carb diet (and not exogenous ketones or MCT), metabolic pathways have been activated and insulin is low. You will be catabolic of your fat tissue.
47:53 You cannot store ketones if insulin is low. If insulin is elevated, even a ketone brought in exogenously, is converted to acetyl CoA and can be stored.
47:57 Hormones drive energy utilization.
51:54 Any cell that you want to maintain and grow requires mTOR. Insulin promotes mTOR activation.
52:55 Leucine is a good mTOR activator in muscle.
53:22 A cancer cell will grow with chronic mTOR activation, but it is not the cause of the cancer.
54:41 Protein consumption does not correlate to cancer incidence. There is evidence that a vegetarian diet, resulting in low levels of LDL. Low LDL is associated with 15 times greater risk of leukemia.
55:41 Animal products are higher in protein and we absorb more. Plants are relatively deficient in protein and we do not absorb it effectively. The longer you live a life with low insulin, the better off you will be. Fasting insulin levels impact Alzheimer’s risk more than age does.
59:17 Carnitine is involved in lipid transport. Longer chain fatty acids need a carnitine shuttle. Low levels of carnitine can be a bottle neck for the mitochondria’s ability to oxidize lipids.
01:00:41 Leucine is the most anabolic amino acid and is a ketogenic amino acid.
01:01:22 Red meat is a great source of carnitine. Carnitine accelerates ketogenesis. We can make our own carnitine. Low carb vegetarians may benefit for supplemental carnitine. Chicken is not a good carnitine source.
01:03:55 Cold induced uncoupling can stimulate mitochondrial uncoupling in muscle. If mitochondria are uncoupled, which means we have mitochondria pulling in glucose and fat and burning it to create heat. Where mitochondria are more tightly coupled, breaking down only enough energy as requested by the cell.
01:05:19 Ketones induce mitochondrial uncoupling in fat tissue, telling it that it is okay to waste energy. In muscle cells, it does not increase mitochondrial uncoupling. It is beneficial for your muscle to only use the energy it needs to use.
01:05:24 Body temperature rises from exercise out of an inherent inefficiency in all chemical reactions.
01:08:56 Cold exposure has an immune benefit and a cognitive benefit, as well as the metabolic benefit.
01:15:39 A main cause of endotoxemia can be LPS (lipopolysaccharide), a membrane component of bacteria. LPS is inhaled or absorbed from the gut. This is accelerated when your body is absorbing lipid.
01:16:47 With lipid absorption, there can be an increase of LPS and endotoxemia. However, dietary lipid consumption also increases LDL. LDL can bind to LPS and result in its removal through the bile duct. Fructose increases LPS, but does not increase LDL.
Related Conversation: Episode #200: Ben Bikman, PhD: Brown Fat Tissue Activation, Insulin & the Ketogenic Diet