Anorexia is a devastating condition that increases risk of death >5X and is associated w/ high rates of relapse
There is desperate need for more effective treatment options
3/10) Common knowledge posits patients w/ anorexia should be discouraged from practicing food group restriction
But anorexia can be framed metabo-psychiatric condition that may benefit from treatment w/ metabolic health interventions w/ neuromodulatory properties, i.e. #ketodiet
4/10) In this case series, we report on 3 patients who -- after having little success with conventional approaches -- went into remission with an animal-based #ketogenic / #carnivore diet
5/10) Patient 1 (female):
👉BMI low 10.7 kg/m2
👉 complicated by starvation hepatitis, osteoporosis, anorexia-induced blindness, and cardiac arrest
👉 Quote: "My high-fat #carnivore diet saved me, and I feel I can now do anything. I'm never going back to the way I was"
6/10) Patient 2 (male):
👉BMI 13
👉 complicated by anxiety, low T, neuropathy, osteopenia
👉 Quote: "But when I started a carnivorous diet, my life changed! My anxiety diminished... I steadily gained weight... I'll never go back."
👉Total testosterone levels ⬆ 6X & free T ⬆ 10X
7/10) Patient 3 (female):
👉BMI low 11.8 kg/m2
👉 Complicated by OCD, depression, self-harm
👉 Quote: "I feel 100% in remission and confident it will stick.”
👉Suffered for 3 decades with treatment-resistant anorexia, before starting #ketogenicdiet; now in remission for > 5 years
8/10) This case series suggest #ketodiet may have clinical utility for some patients with treatment-resistant anorexia, consistent w/ the perspective of eating disorders as “metabo-psychiatric” conditions that can benefit from neuromodulatory interventions, including ketosis
9/10) We hope these cases inspire further research and attract funding for much-needed clinical trials for ketogenic diets for a variety of mental health conditions, including eating disorders.
10/10) YOU can help support this line of research by RETWEETING this thread and sharing the link to the paper on your social media share this thread LINK: insulinresistance.org/index.php/jir/…
🧵1/5): Artificial Sweeteners are Sold Simply as “Sweet without the Calories.”
🤔But while your tongue may get confused, your “Gut Sense” is harder to deceive!
Brilliant work from Diego Bohorquez featured on @hubermanlab shows HOW your body Outsmarts Sweet!
In this thread (please watch vids!), I will walk you through data from a landmark paper that I found awesome – truly, a moment when I say back and went “WOW, our bodies are AMAZING!”
At the end, find the link to the @hubermanlab episode, paper, and FULL VIDEO (11.5 min) breakdown.
cc @R_Mohr @scicommedia @gutbrains
2/5) In this study, the researchers identify “neuropod cells,” which are gastrointestinal cells with nerve-like properties that can sense sweet in the intestines with specific receptors (we will get to what these are in a moment), and then transmit the signal to the brain via the Vagus nerve. (👇jump to 0:56 if you're impatient, like me)
3/5) At this moment, it’s worth taking a detour to explain a technique called “Optogenetics” that these researchers use and that it is becoming increasingly popular to manipulate neuron (and other cell type) activity to prove causality in a system.
⚡️👀Watch clip plz⚡️
In optogenetics, you force specific cells to express channels/pumps on their membranes. The activities of these channels/pumps can be altered by exposure to different wavelengths of light.
Therefore, you can use expression patterns of these channels/pumps, along with different light wavelengths to turn “on” and “off” different cells and circuits.
It’s literally a light switch!
⚡️👀Watch clip plz⚡️
So, using green light they shut off neuropod cells and found that in so doing they could block the response in the Vagus nerve.
Otherwise put, by cutting out singling at the middleman cell – the neuropod cell – they blocked the signal from sugar or sweetener to the Vagus nerve.
This shows that neuropod cells are essential in sensing sweet in the intestines.
This thread is going to ‘wade in,’ drawing inspiration from @hubermanlab w/ @drgabriellelyon + extra information, including NEW 2024 data
🚶♂️The First 3 Will be your Warmup
🏋️♀️Then the Main Set
If you genuinely learn nothing, I’ll buy you a Wagyu Steak.
If you learn at least 3 things, consider a RT of the thread or your most ‘mind-blown’ learning
2/9) #1) We Don’t Know How Much Muscle is Optimal.
At the beginning of the podcast @drgabriellelyon points out a simple but important truth: we don’t know the ideal amount of muscle for a given individual.
Certainly, there’s heterogeneity, but how do we quantify “optimal?”
Optimal for longevity (more on that in #5) Performance? What Type and What Distribution, and how do these impact the endocrine functions of muscles?
There are many unanswered questions with respect to “Muscle-Centric Medicine,” which – I think – makes the field EXCITING!
P.S. Random fact about me, and if you wanted to see what I looked like at 13... and yet I've never been able to bump my BMI above ~22 at max... little boi. Maybe @drgabriellelyon can help, lol:
3/9) #2) Lots of Muscle ≠ Lots of good muscle.
Otherwise stated, Muscle Health is distinct from Muscle Mass. Like a A5 Kobe (delish!), muscle can be large, but ‘sick,’ infiltrated by intramuscular fat. You need sufficient mass to be optimal, but the “Functionality is more important than the Flex.”
Again, measurement and quantification can be difficult. Often, we need to look at proxies, including functional tests but also biomarkers that can be influenced by muscle and its glucose-sink (see 3#!) and endocrine functions.
2/ In this study, normal-weight participants were exposed to EITHER a high-fat/high-sugar snack OR a low-fat/low-sugar snack for 8 weeks in addition to their regular diet. The snacks were to be consumed 2x per day and were isocaloric.
3/ After the intervention, they first tested fat & sugar preferences & found, compared to baseline:
High Fat-Sugar intervention ⬇️ wanting for lowest but also highest fat food
Snacking intervention in general (both high-fat- sugar & low fat-sugar) ⬇️wanting for low sugar food
🚨Carbohydrate insulin model “dead,” OR is it misunderstood again? 🤥
1/ Doctor Tweeted “that the carbohydrate-insulin theory is completely dead” ☠️⚰️
I recently watch the interview with that doctor, and it was surprising the degree to which s/he got the facts wrong…
2/ The CIM does posit that a high glycemic load diet drives high insulin to glucagon ratio state… as a result energy available in the bloodstream is driven downwards in the late postprandial phase leading to “hormonal, hunger” & overeating…
3/ Doc said: “This whole process of fattening all the way down the line, you’ve actually got MORE fuel in your bloodstream… than someone who is not getting fatter.” ... the “decrease EA in the blood "has never been documented because it’s not really there!” Thus, CIM is dead!
1/ How to poo 💩! Was listening to the new @hubermanlab with @DrGottfried this AM (at 3:37) on hormones and #constipation & was inspired to do a little thread on my top #6 tips for dealing with constipation ... hopefully this thread helps at least 1 silent sufferer
2/ This is a topic I'm interested in is bc as someone with a hx of proctitis + cecal patch (form of ulcerative colitis strongly linked to constipation), it's something I've struggled w/ at times. It's not fun & a far more prevalent problem than people realize 4 obvious reasons
3/ Let's start the list.
#1 tip has nothing to do with diet, but technique!
In normal seated position with knees at 90o, your puborectalis muscle strangles your rectum. If you squat with the assistance of a squatty potty (or 'toilet yoga') you receive this strangle-hold