"As a fellow Canadian, Ben, I feel some degree of pride in you. I suppose that is illogical, but there you go. I think there is something fundamentally flawed in the practice of "taking a magic potion" to solve our problems. You are very gifted in explaining to us "Muggles" how eating in an ancestrally appropriate way is the best way to stay healthy and enjoy a more simple life. It feels wrong to have to take a drug to fix the side effects of taking a different drug to solve a problem that does not really need a drug in the first place. Thanks Ben.
Thank you for this assessment. I was looking for the community i trust (low carb) to render an opinion on the GLP1 craze that is sweeping the USA right now. Nice to know that fasting and weight training is not only more effective with less side effects but is also nearly free.
Very interesting. I was glad you mentioned food additcs - I am one - and I have been on Trizepitide (Mounjaro) until recently. It has been VERY helpful to me. I never went on the highest dose. I never felt sick, and I still enjoyed my food, just a lot less of it, AND a lot less carbs too. I had to stop because its too expensive ad so far my weight is not shooting up, tho some cravings have returned. These drugs definitely have a use - ironically here in the UK food addiction isn't recognised (not where I live) and going on the drug privately really has changed my life. When its cheaper I will go back on it at a lower dose. I also smoked less when i was on it?!?!?
They are talking about putting all obese patients on these drugs in the UK. All that would mean is people would never get weight under control. It sounds very expensive and very futile. The same can be done by eating a proper diet. Protein and fat. Limit carbs. Soluble fibre. I dont eat exotic fruits or oils I try to eat the regional food. No seed oils. Glad your letting people know exactly why these GLP 1 are not worth it in the long term. People will clutch them I would have. Before I started Keto. It helps with food cravings.
That was a very informative video. I am on a carnivore diet & have lost 16 kilograms & maintaining this steady weight. I eat OMAD & fast for 20 hours. I’ve met a guy at work who is using a GLP-1 Mounjaro weight loss supplement & seen dramatic results. He’s lost 21kg over 10 weeks. I know that supplement is only a tool for him to get his weight down, I have been doing research this past week to decide whether I should consider this supplement to loose the last 10kg so that my BMI will drop to 25? It’s very thought provoking watching this & listening to your talk. Thank you kindly.
This is.......WOW!!!!!! As usual, there are no shortcuts in the long run. A little help to get over a bump, maybe. The real thing matters. I can also a approve from my own experience that there is no addiction created by either fat nor protein. I am consuming less than 20 grams of carbs daily and I eat, twice a day, to satiety. Weight wise I hover around "set point" XY kg. Same with my wife.
23:00 AUC of insulin is lower, under GLP-1 treatment, but insulin nadir (160-270 min) is higher. Insulin signalling doesn't just relocate GLUT4 to the plasma membrane, it also potentiates the transcription of and activation of acetyl-CoA carboxylase, which catalyzes the conversion of cytosolic citrate to palmitate. The first step of that process produces malonyl-CoA which inhibits long chained fatty acid (LCFA) import into the mitochondria. We can infer then that the insulin nadir is the point of the maximal transport of LCFA across the mitochondrial membranes. Raise the insulin nadir and the fuel line of fatty acids is crimped. Reduce supply of fatty acids and the mitochondria is required to supplement from alternative fuels to support the ATP:ADP ratio. 2 hours after a meal glucose available from circulation has dropped. Where does the mitochondria find fuel when glucose has run low, and fatty acid supply is inhibited. The labile amino acid pool. Now take a process (circulating GLP-1) that was evolutionary conserved to have a half-life of 2 mins, and mess with its degradation so it has a half-life of 2 weeks. And re-dose every week. Of course it causes outsized lean mass loss. How could it do anything else? The best interpretation of the carbohydrate insulin model of obesity must include not just the hormones effect on the source (adipocytes) but also on the sink (LCFA import into beta-oxidation).
Another possibility with a drop in blood glucose levels in diabetics shortly after bariatric surgery is exocrine pancreatic insufficiency (EPI), & carb malabsorption. An early study on Pancreatic Enzyme Replacement Therapy (PERT) supplements given after surgery in diabetics experiencing low blood glucose levels post surgery (eg hypoglycaemia when given pre-surgery insulin injection level regimes) found that PERT supplements alone corrected blood glucose levels, suggesting it was a pancreatic enzyme deficiency & malabsorption issue. Ie, pancreatic enzyme supplements "uncured" the so called diabetes reversal ;)
This was my first thought when I first started seeing the ozempic, wegovy, etc. commercials. "If you or a loved one have taken ozempic..." There is often a price to pay for these indolent "cheat codes"
Thank you .. this is so appreciated... I have struggled with taken GLP1 weight loss drugs.. I work out and play tennis but I am hungry a lot too.. 🙄 anyway- this was very helpful for me to understand how the drugs came about.
He talks about testosterone production in the testes - from another talk here, I thought that was a myth which held until the 90s, and that production actually happened in the adrenal glands. I’m not sure who to believe.
Thank you for mentioning "ADDICTION" to carbs. We literally give sugar to children. Also, won't this ultimately result in a "Sarcopenia Epidemic" in about 20 to 40 years from now?
31:22 Saturated and monounsaturated fats are not only ancestral in our diet, their preferential production and use is heavily conserved in our animal lineage. When we make a fatty acid, we first must make palmitate saturated fatty acid. Only subsequently do we elongate that palmitic into stearic and desaturate that into oleic fatty acid (or desaturate first into palmitoleic, and elongate that into oleic). Further we esterify those fatty acids into fats for transport to storage. The only way a fatty acid can leave the system is through respiration, via beta oxidation. To beta oxidize fatty acids they must be saturated first. Thus above all other considerations saturated fatty acids are our first buffer, and final fuel.
I used to only be able to cook tuna helper. Even I can cook beef, butter, bacon, and eggs. For the eggs, I start with butter in the skillet at 3.5 (out of 10) heat level on my stove so it doesn't burn (your stove may vary). Once the butter is melted, I crack and put in my eggs, then I just watch and wait for the over half of the whites to be opaque, and use a nonstick spatula to flip them. About a minute or 2 later, I put them on my plate. For beef, I use the same skillet and temperature as the eggs. I put a frozen beef patty on the skillet and just wait. One I see tiny spots on the top that have thawed, I put salt and pepper on it then flip it and put salt and pepper on the other side. Again, I just let it sit on the skillet. Once I have seen the juices running from the burger perfectly clear for a minute, I put it on my plate. For bacon, I just microwave thick sliced bacon while everything else is cooking. For my microwave, it generally takes a bit more than a minute per slice.
I'm interested too. Though I've heard only good things about allulose. I tried it before, just as a sweetener before I heard about the GLP1 connection and concluded it was the best tasting sweetener but also about the most expensive. I'm going to try it again and pay attention to hunger.
Sorry but this lecture needs some balance. Providing references relating to type 2 diabetes and not to non-diabetic obesity is a bit misleading, particularly as you have not acknowledged the point verbally. The literature about diabetic usage and side effects - These statistics do not apply to the current trend for weight loss using semaglutide. At 17.20, gastric paresis is cited as a fatal side effect (in type 2 diabetics) and at 20 mins, 2 studies quoted about discontinuation due to side effects (also in type 2 diabetics). These patients are already at risk of gastric paresis due to gut nerve damage. It is fine to cite these statistics in a general lecture about GLP1s but it would be fairer and more balanced to cite the clinical trials and subsequent research on non-diabetic weight loss with semaglutude as well. At 18 minutes, a non-diabetic weight loss usage trial is referenced, and the 40% lean mass statistic is cited. I have not found the 40% statistic in that paper. However, the discussion around body composition in this paper does mention that the proportion of lean mass compared to total body mass is actually increased in the GLP1 patients.
“CHANGE IN BODY COMPOSITION In the DXA subpopulation (140 participants), total fat mass and regional visceral fat mass were reduced from baseline with semaglutide (Table S5). Although total lean body mass decreased in absolute terms (kg), the proportion of lean body mass relative to total body mass increased with semaglutide. SAFETY AND SIDE-EFFECT PROFILE Similar percentages of participants in the semaglutide and placebo groups reported adverse events (89.7% and 86.4%, respectively) (Table 3). Gastrointestinal disorders (typically nausea, diarrhea, vomiting, and constipation) were the most frequently reported events and occurred in more participants receiving semaglutide than those receiving placebo (74.2% vs. 47.9%). Most gastrointestinal events were mild-to-moderate in severity, were transient, and resolved without permanent discontinuation of the regimen (Fig. S8).”
Substitute the phrase ‘time restricted eating’ for fasting to understand the meaning. The purpose is to reduce the number of insulin spikes throughout the day, with the goal of increasing insulin sensitivity / reducing insulin resistance.
The primary benefits of fasting over eating less are: reduced insulin, increased autophagy (helps replace damaged cell parts with healthy ones), more mitochondria (this is how cells create energy), increased growth hormone (this tells the body to burn fat before muscle), and ketosis (this has many benefits on it's own such as reduced inflammation, reduced hunger in overweight people, and better brain/heart function)
First slides very helpful...remainder...your bias again. Please stop referring to 4 yr old studies....how many billions of doses have occurred since then...please stop recycling the old data and trying to use this in your presentations. And if you have no personal experience or clinical experience, walk a mile in our diabetic shoes. Typical professor mindset.
If you want someone to walk a mile in your diabetic shoes before taking their advice, pick any video from Dr Ken Berry MD that talks about the carnivore diet and read the comments. You will find dozens of diabetics that got better without the use of GLP-1 drugs.
The low dose compounded Tirzepatide/glycine/B12 I take has helped break my plateau. Totally agree that if lifestyle changes aren’t made permanently, no diet will succeed long term. As a 53 yo woman, I have lost fat and gained 1 pound of muscle per year for the last 3 years, eating low carb mostly meat, daily restricted eating window, and vigorous exercise. I love your prioritize protein, focus on fasts, control carbs, don’t fear fats. Thank you for your amazing work and sharing of knowledge. 💚🏜️💚
So you lost weight with Tirzepatide and gained a little bit of muscle? So it can be done with a low dose. Thanks for sharing. Were you in the gym a lot doing weights?
The comment about type 1 diabetes people not being able to retain weight absent insulin regardless of calories is an ultimate nail in the CICO coffin
I could listen to Dr. B for hours
Incredible presentation!
Always looking fwd to your next classroom discussions 🤓
Cheers from Switzerland
Brilliant presentation, thanks for sharing.
Thank you Ben for your service and efforts
As usual, Dr. Bikman explained this so well.
Brilliant as always thank you Dr. Bikman.
What a brilliant talk - his students are blessed.
wow, 40% of the weight loss was from lean tissue... that is wild. I had no idea. Thanks for the clear explanations for us regular joes!
As always, Ben is a wealth of information and wisdom
Thank you so much for sharing your information. That’s been very helpful. I really appreciate it.
Thank you for this great presentation!
Excellent presentation.
Thanks Ben. Insightful, as usual.
Excellent video. Thanks.
Brilliant as usual!
This is a brilliant lecture! Thank you so much! 💪🥩💜
"As a fellow Canadian, Ben, I feel some degree of pride in you. I suppose that is illogical, but there you go. I think there is something fundamentally flawed in the practice of "taking a magic potion" to solve our problems. You are very gifted in explaining to us "Muggles" how eating in an ancestrally appropriate way is the best way to stay healthy and enjoy a more simple life. It feels wrong to have to take a drug to fix the side effects of taking a different drug to solve a problem that does not really need a drug in the first place. Thanks Ben.
Thank you for this assessment. I was looking for the community i trust (low carb) to render an opinion on the GLP1 craze that is sweeping the USA right now. Nice to know that fasting and weight training is not only more effective with less side effects but is also nearly free.
Absolutely brilliant lesson Dr Ben 🎉😊❤
Thank you Ben!
Nice talk, thanks for explaining :)
Very interesting. I was glad you mentioned food additcs - I am one - and I have been on Trizepitide (Mounjaro) until recently. It has been VERY helpful to me. I never went on the highest dose. I never felt sick, and I still enjoyed my food, just a lot less of it, AND a lot less carbs too. I had to stop because its too expensive ad so far my weight is not shooting up, tho some cravings have returned. These drugs definitely have a use - ironically here in the UK food addiction isn't recognised (not where I live) and going on the drug privately really has changed my life. When its cheaper I will go back on it at a lower dose. I also smoked less when i was on it?!?!?
They are talking about putting all obese patients on these drugs in the UK.
All that would mean is people would never get weight under control.
It sounds very expensive and very futile.
The same can be done by eating a proper diet.
Protein and fat. Limit carbs. Soluble fibre.
I dont eat exotic fruits or oils I try to eat the regional food. No seed oils.
Glad your letting people know exactly why these GLP 1 are not worth it in the long term.
People will clutch them I would have. Before I started Keto. It helps with food cravings.
Why is soluble fibre necessary in a ketogenic state?
Wonderful and very clear to me a layperson.
Monkeying around with nature's exquisite balancing with pharmaceuticals seldom leads to a good outcome.
Thank you professor Bikman. You gave a very clear and up-to-date summary of the effects, benefits and problems of GLP-1 drugs.
At 20:30 Professor Bikeman answers GLP-1 and insulin levels questions.
That was a very informative video. I am on a carnivore diet & have lost 16 kilograms & maintaining this steady weight.
I eat OMAD & fast for 20 hours.
I’ve met a guy at work who is using a GLP-1 Mounjaro weight loss supplement & seen dramatic results. He’s lost 21kg over 10 weeks.
I know that supplement is only a tool for him to get his weight down, I have been doing research this past week to decide whether I should consider this supplement to loose the last 10kg so that my BMI will drop to 25?
It’s very thought provoking watching this & listening to your talk. Thank you kindly.
Would love to hear the biochemistry with glp1 and harmine! Some really exciting research with beta cell regeneration for t1
This is.......WOW!!!!!!
As usual, there are no shortcuts in the long run. A little help to get over a bump, maybe. The real thing matters.
I can also a approve from my own experience that there is no addiction created by either fat nor protein. I am consuming less than 20 grams of carbs daily and I eat, twice a day, to satiety. Weight wise I hover around "set point" XY kg. Same with my wife.
23:00 AUC of insulin is lower, under GLP-1 treatment, but insulin nadir (160-270 min) is higher.
Insulin signalling doesn't just relocate GLUT4 to the plasma membrane, it also potentiates the transcription of and activation of acetyl-CoA carboxylase, which catalyzes the conversion of cytosolic citrate to palmitate. The first step of that process produces malonyl-CoA which inhibits long chained fatty acid (LCFA) import into the mitochondria. We can infer then that the insulin nadir is the point of the maximal transport of LCFA across the mitochondrial membranes. Raise the insulin nadir and the fuel line of fatty acids is crimped. Reduce supply of fatty acids and the mitochondria is required to supplement from alternative fuels to support the ATP:ADP ratio. 2 hours after a meal glucose available from circulation has dropped. Where does the mitochondria find fuel when glucose has run low, and fatty acid supply is inhibited. The labile amino acid pool.
Now take a process (circulating GLP-1) that was evolutionary conserved to have a half-life of 2 mins, and mess with its degradation so it has a half-life of 2 weeks. And re-dose every week. Of course it causes outsized lean mass loss. How could it do anything else?
The best interpretation of the carbohydrate insulin model of obesity must include not just the hormones effect on the source (adipocytes) but also on the sink (LCFA import into beta-oxidation).
My BMI is 21 and I'm very athletic. My a1c is stubbornly at 5.8
I'm starting 10% carbs eating. I hope it works
Healthy blood cells live longer impacting a1c and giving false impression. How are your other markers such as c-peptide?
Allulose still not approved in Europe 😢
What about berberine? Can you share your thoughts please?
Ben is a genius! ❤
Another possibility with a drop in blood glucose levels in diabetics shortly after bariatric surgery is exocrine pancreatic insufficiency (EPI), & carb malabsorption.
An early study on Pancreatic Enzyme Replacement Therapy (PERT) supplements given after surgery in diabetics experiencing low blood glucose levels post surgery (eg hypoglycaemia when given pre-surgery insulin injection level regimes) found that PERT supplements alone corrected blood glucose levels, suggesting it was a pancreatic enzyme deficiency & malabsorption issue. Ie, pancreatic enzyme supplements "uncured" the so called diabetes reversal ;)
I wonder when the first class action lawsuit will happen
This was my first thought when I first started seeing the ozempic, wegovy, etc. commercials. "If you or a loved one have taken ozempic..." There is often a price to pay for these indolent "cheat codes"
Thank you .. this is so appreciated... I have struggled with taken GLP1 weight loss drugs.. I work out and play tennis but I am hungry a lot too.. 🙄 anyway- this was very helpful for me to understand how the drugs came about.
Great info- Fasting + CV/Ketovore/low carb + weight lifting + some cardio == no drugs needed
If GLP-1 drugs lower blood glucose, could their use be beneficial in cancer treatment?
Seems to me these drugs should be avoided at all costs.
I love your screen name. I, too, am an old cat's lady
Hi Dr Bikman, the leaky gut powder That's very common nowadays, my daughter is taking it, but it contains glp-1, I wonder why? Thanks
Never heard of _"leaky gut powder"._ Is that the actual name? What's the brand?
That’s all wonderful, but what if you can’t eat a high protein diet. Like people who are prone to kidney stones? What is the answer then?
He talks about testosterone production in the testes - from another talk here, I thought that was a myth which held until the 90s, and that production actually happened in the adrenal glands. I’m not sure who to believe.
What does "control" carbs mean?
Why can he just say "Low" carbs. or "Reduce" Carbs.
Interesting
Thank you for mentioning "ADDICTION" to carbs. We literally give sugar to children.
Also, won't this ultimately result in a "Sarcopenia Epidemic" in about 20 to 40 years from now?
There’s no such thing as a free lunch.
31:22 Saturated and monounsaturated fats are not only ancestral in our diet, their preferential production and use is heavily conserved in our animal lineage.
When we make a fatty acid, we first must make palmitate saturated fatty acid. Only subsequently do we elongate that palmitic into stearic and desaturate that into oleic fatty acid (or desaturate first into palmitoleic, and elongate that into oleic). Further we esterify those fatty acids into fats for transport to storage.
The only way a fatty acid can leave the system is through respiration, via beta oxidation. To beta oxidize fatty acids they must be saturated first.
Thus above all other considerations saturated fatty acids are our first buffer, and final fuel.
I just need a way to stop intense sugar cravings, and someone to cook for me, cos I suck at it!
Wishing you the best on your health journey.
I used to only be able to cook tuna helper. Even I can cook beef, butter, bacon, and eggs. For the eggs, I start with butter in the skillet at 3.5 (out of 10) heat level on my stove so it doesn't burn (your stove may vary). Once the butter is melted, I crack and put in my eggs, then I just watch and wait for the over half of the whites to be opaque, and use a nonstick spatula to flip them. About a minute or 2 later, I put them on my plate. For beef, I use the same skillet and temperature as the eggs. I put a frozen beef patty on the skillet and just wait. One I see tiny spots on the top that have thawed, I put salt and pepper on it then flip it and put salt and pepper on the other side. Again, I just let it sit on the skillet. Once I have seen the juices running from the burger perfectly clear for a minute, I put it on my plate. For bacon, I just microwave thick sliced bacon while everything else is cooking. For my microwave, it generally takes a bit more than a minute per slice.
Hmmmm. None of the GLP-1 that I am on, is currently creating nausea.
3 out of 5, because you mentioned calories and “insulin resistance”
GLP1 inhibitor drugs.. "The dose is the poison"... I wonder if the same logic applies to Allulose, which he seems to promote like a salesman.
I'm interested too. Though I've heard only good things about allulose. I tried it before, just as a sweetener before I heard about the GLP1 connection and concluded it was the best tasting sweetener but also about the most expensive. I'm going to try it again and pay attention to hunger.
Sorry but this lecture needs some balance.
Providing references relating to type 2 diabetes and not to non-diabetic obesity is a bit misleading, particularly as you have not acknowledged the point verbally.
The literature about diabetic usage and side effects - These statistics do not apply to the current trend for weight loss using semaglutide.
At 17.20, gastric paresis is cited as a fatal side effect (in type 2 diabetics) and at 20 mins, 2 studies quoted about discontinuation due to side effects (also in type 2 diabetics). These patients are already at risk of gastric paresis due to gut nerve damage.
It is fine to cite these statistics in a general lecture about GLP1s but it would be fairer and more balanced to cite the clinical trials and subsequent research on non-diabetic weight loss with semaglutude as well.
At 18 minutes, a non-diabetic weight loss usage trial is referenced, and the 40% lean mass statistic is cited. I have not found the 40% statistic in that paper. However, the discussion around body composition in this paper does mention that the proportion of lean mass compared to total body mass is actually increased in the GLP1 patients.
“CHANGE IN BODY COMPOSITION
In the DXA subpopulation (140 participants), total fat mass and regional visceral fat mass were reduced from baseline with semaglutide (Table S5). Although total lean body mass decreased in absolute terms (kg), the proportion of lean body mass relative to total body mass increased with semaglutide.
SAFETY AND SIDE-EFFECT PROFILE
Similar percentages of participants in the semaglutide and placebo groups reported adverse events (89.7% and 86.4%, respectively) (Table 3). Gastrointestinal disorders (typically nausea, diarrhea, vomiting, and constipation) were the most frequently reported events and occurred in more participants receiving semaglutide than those receiving placebo (74.2% vs. 47.9%). Most gastrointestinal events were mild-to-moderate in severity, were transient, and resolved without permanent discontinuation of the regimen (Fig. S8).”
Thumbs up from a keto-rebel.
"Disease of prosperity"
BEN BIKMAN FOR PRESIDENT!❤🎉
Isn’t fasting the literal definition of eating less? But eating less doesn’t work? But fasting works?
Head spinning to the contradictions
The "eat less, move more" mantra is intended to be a permanent lifestyle. Fasting is for a day or maybe a week with special effort.
Substitute the phrase ‘time restricted eating’ for fasting to understand the meaning. The purpose is to reduce the number of insulin spikes throughout the day, with the goal of increasing insulin sensitivity / reducing insulin resistance.
The primary benefits of fasting over eating less are: reduced insulin, increased autophagy (helps replace damaged cell parts with healthy ones), more mitochondria (this is how cells create energy), increased growth hormone (this tells the body to burn fat before muscle), and ketosis (this has many benefits on it's own such as reduced inflammation, reduced hunger in overweight people, and better brain/heart function)
You may want to start right off by telling viewers what GLP-1 drugs are.
❤
First slides very helpful...remainder...your bias again. Please stop referring to 4 yr old studies....how many billions of doses have occurred since then...please stop recycling the old data and trying to use this in your presentations. And if you have no personal experience or clinical experience, walk a mile in our diabetic shoes. Typical professor mindset.
If you want someone to walk a mile in your diabetic shoes before taking their advice, pick any video from Dr Ken Berry MD that talks about the carnivore diet and read the comments. You will find dozens of diabetics that got better without the use of GLP-1 drugs.
The low dose compounded Tirzepatide/glycine/B12 I take has helped break my plateau. Totally agree that if lifestyle changes aren’t made permanently, no diet will succeed long term. As a 53 yo woman, I have lost fat and gained 1 pound of muscle per year for the last 3 years, eating low carb mostly meat, daily restricted eating window, and vigorous exercise. I love your prioritize protein, focus on fasts, control carbs, don’t fear fats. Thank you for your amazing work and sharing of knowledge. 💚🏜️💚
So you lost weight with Tirzepatide and gained a little bit of muscle? So it can be done with a low dose. Thanks for sharing. Were you in the gym a lot doing weights?