Given the controversy around Guyenet's view that weight change is a simple function of calories in and energy consumed, I was surprised to see him postulate it at the start of his talk. Presenting it as self-evident and indicating that he would not discuss it at all put me off right away. I also noted a number of instances later on in which he seemed to conflate correlation with causation. I agree with Stavia that his presentation was not especially ambitious, and I too am not persuaded that it's all about the calories.
In contrast, I think Dr. Masterjohn and Dr. Bredesen gave authoritative, fascinating, and highly credible presentations. I also think Kyle Mamounis gave a terrific talk with the provocative thesis, "Fatty Acids in Obesity and Disease: The Case Against Being a Fat Burner". I'm a sucker for speakers who convey passion for science as an ongoing learning process and who communicate their own skepticism about available evidence with care and nuance.
2016 Ancestral Health Meetup - Stavia's blog
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progranulindefect
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Re: 2016 Ancestral Health Meetup - Stavia's blog
"And he also cited the Diabetes Prevention Program Study which showed for every kg lost in a prediabetic there was a 16% reduction in progression to type 2 diabetes."
weight loss doesn't always help. my a1c in 2009 was 5.9 at 143 pounds and 5'3''. then i lost weight on the paleo diet, but i was still eating a lot of fruit. i got to 129 pounds (high school weight) and an A1c of 5.7 (still prediabetic). now i am 137 pounds and my A1c is 5.4 (low carb, but more fat- maybe too much fat- and nearing menopause at 51).
weight loss doesn't always help. my a1c in 2009 was 5.9 at 143 pounds and 5'3''. then i lost weight on the paleo diet, but i was still eating a lot of fruit. i got to 129 pounds (high school weight) and an A1c of 5.7 (still prediabetic). now i am 137 pounds and my A1c is 5.4 (low carb, but more fat- maybe too much fat- and nearing menopause at 51).
AARON BLAISDELL
Diet and cognition: data, theory and some solutions from the playbook of psychology: Detrimental effects of low fat diet and rats' cognition placed in the greater context of psychological theory and phenomena. Psychological solutions for diet related health problems
Aaron has studied the effects of diet on rat cognition and mood. There are striking reductions in motivation, impulse control, vigilance, working memory, hippocampal memory, integrity of hippocampal blood brain barrier and spatial learning with a highly refined diet as opposed to a whole foods diet.
In humans pathways to this have been identified and include increased inflammation through cytokine activation which then dysregulates neurotransmitters and neuromodulators. Inflammatory mediated depression resembles sickness behavior with withdrawal and energy conservation as opposed to anhedonia.
Refined foods are also shown to increase anxiety most likely through micronutrient deficiency eg Zinc Magnesium Lithium and Chromium.
Why do we eat refined foods?
1.Supernormal Stimuli : a bird will nest on a giant egg in preference to the normal size. Supernormal stimuli will override normal stimuli - refined foods are hyperpalatable. and elicit consummatory responses larger than are elicited by whole foods. thus leading to overcomsumption and dysregulation of appetite
2. Pavlovian Response: we learn to like foods based on Pavlovian preferences. Refined foods are calorie dense thus drive association stronger than whole foods
3. Habit Learning: as we learn a skill we turn it into a habit and it becomes automatic eg driving. Refined foods accelerate and strengthen habit learning. There are more neurones in the basal ganglia of obese persons in areas that code for value and saliency of food
4. Delay Discounting: we discount rewards that are too far in the future or when the immediate reward is too enticing
5. Learned Helplessness: this is the curse of yoyo dieting - repeated unsuccessful attempts to lose weight results in feelings of helplessness
6. Overshadowing: We all know the Pavlovian dog response to the bell. However if there are multiple cues the loudest overshadows the quieter - refined foods overshadow whole foods due to their stronger stimulus
7. Counterconditioning of bad tastes: chemicals taste awful but their pairing with sugar they start to taste good
8. Sensory Adaptation and Habituation: Overstimulation causes down regulation of receptors (e.g. down regulation of tongue sweet receptors with repeated ingestion of sugar rich foods) and habituation (one gets used to feeling unwell with a diet of refined foods)
What can we do?
1.Extinction of food cue responses: presenting a food without eating will eventually break the prior association of that cue with food - looking and smelling without eating.
2. Break food cravings : Seth Roberts discovered that eating calories without flavour or taste decreases body fat set point - this can be achieved by drinking EVOO for calories or eating with a clothes peg on the nose. This works through Pavlovian reconditioning
3. Reward devaluation: devaluing refined foods can help us mentally avoid seeking them out - mentally devalue junk food and develop an aversion for it
4. Equivalence class formation: we all classify objects into categories - we can reclassify junk food as toxic non-food
5. Cultivate new eating habits: make a habit of avoiding refined foods and eating whole foods
6. Mindful eating: suggestions are choosing only whole foods, drinking only water, coffee, tea, moderate alcohol, eat only at the meal table not while distracted, keep snacks in pantry not in plain view, keep fruits and nuts as snacks, eat slowly and taste your food, if a craving develops, go for a walk
7. Social support! This is what we do here!
8. Redefine yourself as someone who does not eat junk food
He ended by saying that rats were better at the studied mood and cognition parameters after 5 weeks off the junk food.
My opinion: brilliant talk. Susan and I are going to develop a version for our beginners forum as we realized this is an area we have not yet addressed: how to sustain changes in lifestyle.
Diet and cognition: data, theory and some solutions from the playbook of psychology: Detrimental effects of low fat diet and rats' cognition placed in the greater context of psychological theory and phenomena. Psychological solutions for diet related health problems
Aaron has studied the effects of diet on rat cognition and mood. There are striking reductions in motivation, impulse control, vigilance, working memory, hippocampal memory, integrity of hippocampal blood brain barrier and spatial learning with a highly refined diet as opposed to a whole foods diet.
In humans pathways to this have been identified and include increased inflammation through cytokine activation which then dysregulates neurotransmitters and neuromodulators. Inflammatory mediated depression resembles sickness behavior with withdrawal and energy conservation as opposed to anhedonia.
Refined foods are also shown to increase anxiety most likely through micronutrient deficiency eg Zinc Magnesium Lithium and Chromium.
Why do we eat refined foods?
1.Supernormal Stimuli : a bird will nest on a giant egg in preference to the normal size. Supernormal stimuli will override normal stimuli - refined foods are hyperpalatable. and elicit consummatory responses larger than are elicited by whole foods. thus leading to overcomsumption and dysregulation of appetite
2. Pavlovian Response: we learn to like foods based on Pavlovian preferences. Refined foods are calorie dense thus drive association stronger than whole foods
3. Habit Learning: as we learn a skill we turn it into a habit and it becomes automatic eg driving. Refined foods accelerate and strengthen habit learning. There are more neurones in the basal ganglia of obese persons in areas that code for value and saliency of food
4. Delay Discounting: we discount rewards that are too far in the future or when the immediate reward is too enticing
5. Learned Helplessness: this is the curse of yoyo dieting - repeated unsuccessful attempts to lose weight results in feelings of helplessness
6. Overshadowing: We all know the Pavlovian dog response to the bell. However if there are multiple cues the loudest overshadows the quieter - refined foods overshadow whole foods due to their stronger stimulus
7. Counterconditioning of bad tastes: chemicals taste awful but their pairing with sugar they start to taste good
8. Sensory Adaptation and Habituation: Overstimulation causes down regulation of receptors (e.g. down regulation of tongue sweet receptors with repeated ingestion of sugar rich foods) and habituation (one gets used to feeling unwell with a diet of refined foods)
What can we do?
1.Extinction of food cue responses: presenting a food without eating will eventually break the prior association of that cue with food - looking and smelling without eating.
2. Break food cravings : Seth Roberts discovered that eating calories without flavour or taste decreases body fat set point - this can be achieved by drinking EVOO for calories or eating with a clothes peg on the nose. This works through Pavlovian reconditioning
3. Reward devaluation: devaluing refined foods can help us mentally avoid seeking them out - mentally devalue junk food and develop an aversion for it
4. Equivalence class formation: we all classify objects into categories - we can reclassify junk food as toxic non-food
5. Cultivate new eating habits: make a habit of avoiding refined foods and eating whole foods
6. Mindful eating: suggestions are choosing only whole foods, drinking only water, coffee, tea, moderate alcohol, eat only at the meal table not while distracted, keep snacks in pantry not in plain view, keep fruits and nuts as snacks, eat slowly and taste your food, if a craving develops, go for a walk
7. Social support! This is what we do here!
8. Redefine yourself as someone who does not eat junk food
He ended by saying that rats were better at the studied mood and cognition parameters after 5 weeks off the junk food.
My opinion: brilliant talk. Susan and I are going to develop a version for our beginners forum as we realized this is an area we have not yet addressed: how to sustain changes in lifestyle.
Re: 2016 Ancestral Health Meetup - Stavia's blog
NORA GEDGAUDAS
Is there one truly optimal, universally foundational human diet - bio-individuality as a secondary not a primary issue.
Exploring the way is which our seemingly diverse human population is far more alike than unalike and the prioritisation of foundational needs versus bio-individual needs and polymorphisms.
Nora asked the question of if we are truly all different? She used as her basis for refutation of this the fact that there is one anatomy and physiology textbook for all humans and she feels we are more alike than non-alike and there is not a lot of wiggle room. Using the work of Weston A Price she distilled the diets of the peoples he studies and looked for the commonalities which she feels are that these societies eat as many animal sources of of food as they possibly can and in addition the most valued foods are fats. She added to this the opinion that the human body has zero requirement for dietary carbohydrates and concluded that the optimal diet is solely animal based and that the bonus is a variety of fibrous veggies and greens.
She cited the Inuit as proof of her hypothesis.
My feelings: cherry picking (I looked up the Inuit evidence myself during the talk and it did not tally with her version), dogmatic, glossing over a very complex area. Not impressed.
Is there one truly optimal, universally foundational human diet - bio-individuality as a secondary not a primary issue.
Exploring the way is which our seemingly diverse human population is far more alike than unalike and the prioritisation of foundational needs versus bio-individual needs and polymorphisms.
Nora asked the question of if we are truly all different? She used as her basis for refutation of this the fact that there is one anatomy and physiology textbook for all humans and she feels we are more alike than non-alike and there is not a lot of wiggle room. Using the work of Weston A Price she distilled the diets of the peoples he studies and looked for the commonalities which she feels are that these societies eat as many animal sources of of food as they possibly can and in addition the most valued foods are fats. She added to this the opinion that the human body has zero requirement for dietary carbohydrates and concluded that the optimal diet is solely animal based and that the bonus is a variety of fibrous veggies and greens.
She cited the Inuit as proof of her hypothesis.
My feelings: cherry picking (I looked up the Inuit evidence myself during the talk and it did not tally with her version), dogmatic, glossing over a very complex area. Not impressed.
Re: 2016 Ancestral Health Meetup - Stavia's blog
STEVEN GUNDRY
Dietary management of the Apoe4 genotype, the true ancestral gene
Focus of reducing small dense oxidizable LDL particles via a low animal fat, high soluble fibre and resistant starch diet as well as using generous amounts of polyphenol rich olive oil, resveratrol, grape seed extract, turmeric and pomegranate seed oil.
Dr Gundry was the first of the apoe4 speakers and was greeted with raucous applause by three rows of us in the front. I think I heard cheers as well. He spoke very well and we were gratified to see the hall almost full of paleo folks - of whom at least 20% will be e4 carriers.
He reiterated his approach to what he called the true ancestral allele. His views are well known and on his website. We all know his approach focused on keeping small dense oxidizable LDL minimal by limiting animal fats and proteins, generous amounts of polyphenols, no grains or lectins, emphasis on shellfish and fibrous veggies. He is in favour of several supplements such as niacinamide, resveratrol, pycnogenol, grape seed extract, Omega3's and many others which are found elsewhere on our site. He is not in favor of coconut as he has seen it raise small dense LDL. He feels raised IgF1 accelerates aging. He feels MCT is neutral.
My opinion: he spoke very well and presented his approach in a very accessible way.
Dietary management of the Apoe4 genotype, the true ancestral gene
Focus of reducing small dense oxidizable LDL particles via a low animal fat, high soluble fibre and resistant starch diet as well as using generous amounts of polyphenol rich olive oil, resveratrol, grape seed extract, turmeric and pomegranate seed oil.
Dr Gundry was the first of the apoe4 speakers and was greeted with raucous applause by three rows of us in the front. I think I heard cheers as well. He spoke very well and we were gratified to see the hall almost full of paleo folks - of whom at least 20% will be e4 carriers.
He reiterated his approach to what he called the true ancestral allele. His views are well known and on his website. We all know his approach focused on keeping small dense oxidizable LDL minimal by limiting animal fats and proteins, generous amounts of polyphenols, no grains or lectins, emphasis on shellfish and fibrous veggies. He is in favour of several supplements such as niacinamide, resveratrol, pycnogenol, grape seed extract, Omega3's and many others which are found elsewhere on our site. He is not in favor of coconut as he has seen it raise small dense LDL. He feels raised IgF1 accelerates aging. He feels MCT is neutral.
My opinion: he spoke very well and presented his approach in a very accessible way.
Re: 2016 Ancestral Health Meetup - Stavia's blog
DALE BREDESEN
Apoe4 mechanistics and a protocol for the reversal of cognitive decline
Description of a comprehensive therapeutic program to reverse cognitive decline in SCI, MCI and early AD.
Dale spoke eloquently and with authority about his program for prevention and reversal of cognitive decline.
We all know it very well, his findings of the apoe4 molecule binding to cell membrane receptors, interacting with RelA (a pro-inflammatory mediator) and enters the nucleus. Here it binds to 1800 gene promotors and these effects resultin increase in NFkB and decrease in SIRT1. This is a pro-inflammatory state as opposed to a SIRT1 dominant anti-inflammatory state.
This is the ancestral allele. Apoe3 appeared around 220 000 years ago and Apoe2 only 70 to 80 000 years ago. Apoe2, being a dominant inflammatory state, has advantages in a situation of living in the bush, waking barefoot, eating carrion, fighting over resources. Also of note is that E4s tend to be hyperabsorbers of fats. This is hugely advantageous in times of famine as reserves will be higher, however not so good in the context of our present abundance of food.
In today's environment, Dale and his team have identified 36 "holes in the roof " which he uses as a metaphor for detrimental downstream effects resulting in dementia. There are complex interactions involving glucose homeostasis, microtubule disassembley, inflammation, neurotrophins and cell death, synapse dysfunction. He feels amyloid is a protective response to three main stressors-1. inflammation both infectious and sterile (HSV, EBV, CMV, biofilms/ AGE modified molecules) - 2. withdrawal of trophic support (nerve growth factor, estrogen, testosterone, D3 )- and 3. response to toxins (eg mercury, mycotoxins)
He calls these types 1 2 and3. There is also an intermediate group 1.5which he calls glycotoxic. Here AGEs cause inflammation which leadsto insulin resistance thus with IR trophic support is effectively lacking.
He also has shown that in a trophic support environment the amyloid precursor molecule is cleaved into two functional parts. In an antitrophic environment it is cleaved into smaller fragments, one of which is abeta which unfortunately seems to accumulate in a prionic-like manner. The downstream effect is accumulated amyloid, tau and mitochondrial dysfunction.
He then described his program which we all know very well.
My opinion: brilliant as always, clearly at the top of his game and likely the world's top expert in the field of Alzheimers. A privilege to hear him speak.
Apoe4 mechanistics and a protocol for the reversal of cognitive decline
Description of a comprehensive therapeutic program to reverse cognitive decline in SCI, MCI and early AD.
Dale spoke eloquently and with authority about his program for prevention and reversal of cognitive decline.
We all know it very well, his findings of the apoe4 molecule binding to cell membrane receptors, interacting with RelA (a pro-inflammatory mediator) and enters the nucleus. Here it binds to 1800 gene promotors and these effects resultin increase in NFkB and decrease in SIRT1. This is a pro-inflammatory state as opposed to a SIRT1 dominant anti-inflammatory state.
This is the ancestral allele. Apoe3 appeared around 220 000 years ago and Apoe2 only 70 to 80 000 years ago. Apoe2, being a dominant inflammatory state, has advantages in a situation of living in the bush, waking barefoot, eating carrion, fighting over resources. Also of note is that E4s tend to be hyperabsorbers of fats. This is hugely advantageous in times of famine as reserves will be higher, however not so good in the context of our present abundance of food.
In today's environment, Dale and his team have identified 36 "holes in the roof " which he uses as a metaphor for detrimental downstream effects resulting in dementia. There are complex interactions involving glucose homeostasis, microtubule disassembley, inflammation, neurotrophins and cell death, synapse dysfunction. He feels amyloid is a protective response to three main stressors-1. inflammation both infectious and sterile (HSV, EBV, CMV, biofilms/ AGE modified molecules) - 2. withdrawal of trophic support (nerve growth factor, estrogen, testosterone, D3 )- and 3. response to toxins (eg mercury, mycotoxins)
He calls these types 1 2 and3. There is also an intermediate group 1.5which he calls glycotoxic. Here AGEs cause inflammation which leadsto insulin resistance thus with IR trophic support is effectively lacking.
He also has shown that in a trophic support environment the amyloid precursor molecule is cleaved into two functional parts. In an antitrophic environment it is cleaved into smaller fragments, one of which is abeta which unfortunately seems to accumulate in a prionic-like manner. The downstream effect is accumulated amyloid, tau and mitochondrial dysfunction.
He then described his program which we all know very well.
My opinion: brilliant as always, clearly at the top of his game and likely the world's top expert in the field of Alzheimers. A privilege to hear him speak.
Re: 2016 Ancestral Health Meetup - Stavia's blog
Jumping ahead to dinner #2, we have just reluctantly left another stunning evening, this time honouring Dr Gundry who has so generously spent this time with us.
He shared his insights on lectins and other drivers of pathology. He has certainly given me personally much food for thought and I could see everyone was engaged similarly.
It was a special moment to see him, Dr Terry Wahls and Dr Dale Bredesen in animated discussion. What a treat and we have to thank Julie for achieving this wonderful event.
Theresa and George have again very kindly recorded it and I am sure when they are home they will load it here.
He shared his insights on lectins and other drivers of pathology. He has certainly given me personally much food for thought and I could see everyone was engaged similarly.
It was a special moment to see him, Dr Terry Wahls and Dr Dale Bredesen in animated discussion. What a treat and we have to thank Julie for achieving this wonderful event.
Theresa and George have again very kindly recorded it and I am sure when they are home they will load it here.
Re: 2016 Ancestral Health Meetup - Stavia's blog
As promised, here is the recording from tonight's Q&A session with Dr Steven Gundry.
Dr Gundry's dinner Q&A session at AHS Aug 12, 2016
Dr Gundry's dinner Q&A session at AHS Aug 12, 2016
Last edited by TheresaB on Tue Aug 16, 2016 9:26 pm, edited 1 time in total.
-Theresa
ApoE 4/4
ApoE 4/4
Re: 2016 Ancestral Health Meetup - Stavia's blog
Theresa you are wonderful!! Thank you!!
Re: 2016 Ancestral Health Meetup - Stavia's blog
ok back to Day 1
RAND AKASHEH
Alzheimers disease: pathophysiology and nutritional implications: Role of glucose, lipids and ketone bodies in pathogenesis, prevention and management of AD, through mechanisms controlling nutrient transport in healthy and diseased brains
What causes an imbalance between protein formation and recycling? Associated factors for AD point to diabetes and increased insulin as a major risk factor.
The brain consumes 20 to 30% of the bodies energy. Substrates for the Krebs cycle are glucose (from food or gluconeogenesis), ketone bodies, lactate and MCTs.
In Alzheimers there is both reduced glucose uptake as well as cerebral insulin resistance with down regulation of receptors. There is proven ~20 to 25% decrease in glucose metabolism in the hippocampus in early AD and in other areas such as frontal, temporal and parietal lobes in later AD. Mechanisms include reduced expression of GLUT1 and 3, ineffective Krebs cycle and mitochondrial dysfunction (explains the maternal inheritance). This induces tau hyperphosphorylation which impairs neurotransmission.
It is critical to realise brain insulin resistance can occur in the absence of peripheral insulin resistance, obesity and diabetes.
Ketones can provide up to 60% of the brain's energy requirements. Mild ketonaemia of 0.4 to 0.5mmol/l can contribute 5 to 10% of energy needs. Production of endogenous ketones during fasting is dependent on optimal blood glucose and insulin levels. Insulin directly inhibits ketogenesis. Low insulin directly initiates lipolysis, fatty acids go to the liver and are beta oxidised to ketone bodies which then enter the blood and are transported to the brain etc.
She stressed that a high fat low carb diet may not necessarily induce ketosis if insulin resistance is present. This needs to be addressed first by weight loss, exercise, fasting etc
She also discussed the role of IDE (insulin degrading enzyme) which has a role in degrading many other proteins other than insulin , especially relevant is that it degrades amyloid. High circulating insulin will preferentially bind to it so there is less available to degrade amyloid.
My comments: guys, I am constantly saying glycaemic control trumps lipids. Every.single.time. You have been brainwashed by media. Lipids are important but so so so much less than insulin/glucose.
Warning rant: I so often see our new members introduce themselves and the first biomarker they share is their lipid profile. We need to focus on the top strategies in our hierarchy of dietary aims: glycaemic control and inflammation. Rant over.
She was brilliant and did especially well following Drs Gundry and Bredesen.
RAND AKASHEH
Alzheimers disease: pathophysiology and nutritional implications: Role of glucose, lipids and ketone bodies in pathogenesis, prevention and management of AD, through mechanisms controlling nutrient transport in healthy and diseased brains
What causes an imbalance between protein formation and recycling? Associated factors for AD point to diabetes and increased insulin as a major risk factor.
The brain consumes 20 to 30% of the bodies energy. Substrates for the Krebs cycle are glucose (from food or gluconeogenesis), ketone bodies, lactate and MCTs.
In Alzheimers there is both reduced glucose uptake as well as cerebral insulin resistance with down regulation of receptors. There is proven ~20 to 25% decrease in glucose metabolism in the hippocampus in early AD and in other areas such as frontal, temporal and parietal lobes in later AD. Mechanisms include reduced expression of GLUT1 and 3, ineffective Krebs cycle and mitochondrial dysfunction (explains the maternal inheritance). This induces tau hyperphosphorylation which impairs neurotransmission.
It is critical to realise brain insulin resistance can occur in the absence of peripheral insulin resistance, obesity and diabetes.
Ketones can provide up to 60% of the brain's energy requirements. Mild ketonaemia of 0.4 to 0.5mmol/l can contribute 5 to 10% of energy needs. Production of endogenous ketones during fasting is dependent on optimal blood glucose and insulin levels. Insulin directly inhibits ketogenesis. Low insulin directly initiates lipolysis, fatty acids go to the liver and are beta oxidised to ketone bodies which then enter the blood and are transported to the brain etc.
She stressed that a high fat low carb diet may not necessarily induce ketosis if insulin resistance is present. This needs to be addressed first by weight loss, exercise, fasting etc
She also discussed the role of IDE (insulin degrading enzyme) which has a role in degrading many other proteins other than insulin , especially relevant is that it degrades amyloid. High circulating insulin will preferentially bind to it so there is less available to degrade amyloid.
My comments: guys, I am constantly saying glycaemic control trumps lipids. Every.single.time. You have been brainwashed by media. Lipids are important but so so so much less than insulin/glucose.
Warning rant: I so often see our new members introduce themselves and the first biomarker they share is their lipid profile. We need to focus on the top strategies in our hierarchy of dietary aims: glycaemic control and inflammation. Rant over.
She was brilliant and did especially well following Drs Gundry and Bredesen.
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