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Nick Norwitz

@nicknorwitz

Jan 16

Layne’s 'Steaking' a Claim on #Carnivore. Let’s assess the rigor of his claims in a brief thread 🧵🥩👇

1/5) First, @BioLayne engages in ‘superficial citation bombing,’ a tactic whereby an influencer drops and bunch of references (here, in the form of pubmed IDs), without doing his due diligence to process the data. Here, he qualifies carnivore diet as extreme keto (and basically zero carb), but then cites studies where the ‘low-carb’ threshold is 40-45% kCal.

The meta-analysis he cites classified “low-carbohydrate diet” as ≤40% kCal from carbs with fat kCals as low as 30% (Table 1, PMID: 32238384)

Similarly, the Cochrane review he cites includes low-carb diets “< 45%” kCal from carbs.

There is a sub-section on ‘very-low carb diets’ (on which he does not comment). Largely, this was qualitative in the report.

But if you actually dig into the RCTs, you’ll note results like, “In a 12-month trial, adults with elevated HbA1c and body weight assigned to an low-carbohydrate ketogenic diet had greater reductions in HbA1c, lost more weight, and reduced more medications than those instructed to follow an moderate-carbohydrate, calorie-restricted, low-fat diet.” (PMID: 29269731)

This is par for the course with Layne. He once tried to dunk on me citating a paper where it was very clear he didn’t look at Figure 1.

*Note 1: I can't quote his Tweet because I remain blocked*

*Note 2: As I've made abundantly clear, I'm more than happy to engage in a long-form discussion / debate with Layne. He's declined every opportunity in the past.*

2/5) He calls a carnivore diet “unnecessary” and “not backed by any scientific evidence.”

But, as any good scientist should know, “absence of evidence is not evidence of absence.” Furthermore “necessary” deserves qualification. Let’s start with the latter.

Is a carnivore diet “necessary” to lose weight. No. Who said it was?

However, clinical reports (and case series, PMID: 39296504) suggest that for some patients a carnivore diet is ‘necessary’ (or uniquely beneficial) to keep their specific clinical conditions (e.g. inflammatory bowel disease) in remission.

Having met, interviewed and taken medical histories on these patients (including those with decades suffering with disease and trialing all form of immunomodulators etc., only to find relief with a carnivore diet), I feel comfortable for saying – yes – a carnivore diet may be ‘necessary’ for these patients to live a tolerable life.

Does that mean carnivore is the best diet? No.

Does it mean that fiber is bad for your average person? No.

But to sweep under the rug the metabolic use cases where a carnivore diet may prove uniquely beneficial is uncurious and anti-scientific.

Now, to the “absence of evidence is not evidence of absence” statement. It’s true, there aren’t RCTs on carnivore diet for X condition. Why? They haven’t been funded and run.

So to say “not backed by any scientific evidence” is technically true but overlooks the important and practical fact that “more research is needed” before a carnivore diet could be recommended as standard of care.

3/5) It does not take a PhD (a fact "Dr" Norton never misses a chance to flex, including in his recent thread) to evaluate what @BioLayne is doing. It's what he usually does: 'attack the other' to garner clicks and social media points rather than actually trying to engage on the issues with any degree of nuance.

For those who don't know, when I first began to engage with Layne I was optimistic I could get his to the table for a serious discussion about complex matters.

But, again and again, he avoided/declined long-form verbal engagement and instead opted for shallow one-sided attacks.

For more on my assessment of his behavioral patterns, you can start here: youtu.be/iZ4p1bCsUio

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Nick Norwitz

@nicknorwitz

Jan 10

🚨 BIG Paper and BIG Initiative, CME-Credits! 🚨

1/4) 🍩🦠 Today’s video covers breaking new research in Nature Metabolism about a Virus that Causes Food Addiction?!

But that’s not all! I’m proud to be collaborating with Metabolic Health Initiative—the ACCME-accredited medical education organization behind The Metabolic Health Summit @MetabolicSummit, and The Metabolic Link podcast. Together, we are working to get some of my content CME-accredited, including this video!

This creates an incentive for doctors to learn about metabolic health, as part of our broader efforts to Make Metabolic Health Mainstream! Read on, then Spread the Word!

2/4) Here's a review of findings in 4 Quick Points:
👉 A particular Microviridae virus can infect gut bacteria
👉 In so doing, the virus alters the metabolism of dopamine and serotonin precursors
👉 This is linked to changes in brain activity, on fMRI, and worse Food Addiction Scores
👉 "Fecal Viral Transplant" Experiments suggest a causal relationship between this virus and food addiction behavior

Thus, these data suggest an axis whereby a virus can contribute to the clinical signs of food addiction, a big step in demystifying the link between gut-brain and eating behavior

For details (and to hear from the senior author of this research), see link in 3/4

3/4) For more nuances, and to hear directly, from the senior author of this groundbreaking research, check out the full video, here:

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Nick Norwitz

@nicknorwitz

Jan 7

🍩🧬Carbs and Codons: Understand Your Genes to Defeat Obesity 🧬🍩

1/6) This thread 🧵 review Mendelian Randomization that supports the Carbohydrate Insulin Model (#CIM) of Obesity. Let's dive in!

Background on Terms: CIM and Mendelian Randomization👇

🍩 The CIM is a mechanistic model of obesity that works as follows: a high glycemic load diet (meaning one that tends to spike blood sugar and blood insulin levels more) gives a hormonal signal to the body (high insulin) to store energy as fat tissue.

In other words, energy (calories) come in, and they’re “triaged:” preferentially towards fat, rather than energy expenditure or lean tissue.

As a downstream consequence, energy expenditure goes down and hunger increases. Thus, while “calories in – calories out = weight change” and thermodynamics is maintained, the calorie imbalance is the result of a primary hormonal disturbance.

🧬 Mendelian Randomization

A method scientists use to study whether a certain factor (like insulin secretion) causes a particular outcome (in this case, obesity).

It relies on genetic variations (remember those 4 million variable genetics sites?) that are assigned randomly by nature’s genetic coin toss to uncover cause-and-effect relationships.

🚨Study Question

So, in this study, the researchers asked the question, “does carbohydrate-stimulated insulin secretion (the amount of insulin released in response to a carbohydrate load) predict obesity?”

ht/ @davidludwigmd cc @AdrianSotoMota @drjasonfung @drericwestman @DaveEDanna @realDaveFeldman @ChrisPalmerMD @janellison
#MendelianRandomization #Genetics #Lowcarb

2/6) In this study, they used MAGIC! No, actually, they relied on data from the Meta-Analysis of Glucose- and Insulin-related traits Consortium (MAGIC), a previously published meta-analyses on insulin secretion including 26,037 people.

They also used data from the United Kingdom Biobank (n =138,541), and a validation cohort, the Cardiology and Metabolic Patient Cohort study at Massachusetts General Hospital (n =1,675).

Using prior knowledge about variations in the human genome, they created genetic risk scores for the traits: (i) carbohydrate-stimulated insulin secretion (how much insulin a person secretes in response to carbs), and (ii) body mass index (BMI).

3/6) The researchers found a higher insulin release genetic risk scores did predict higher BMI.

In fact, they even tested slightly different insulin release genetic risk scores in different populations and consistently found - “Yes!” - more insulin release in response to carbs, as influenced by genetics, did predict a higher BMI.

This is consistent with the #CIM: where higher insulin release tells fat cells to store fat, leading to obesity. This puts calories in the passenger seat where a calorie imbalance results, not from “just eating too many calories,” but from the hormonally stimulated growth of fat cells.

Read 6 tweets

Nick Norwitz

@nicknorwitz

Jan 6

🚨GLP-1: “It’s Not That Simple”💉

1/4) There are many strong, often dogmatic, opinions on GLP-1 receptor agonists. One interesting, and under-appreciated, fact is that GLP-1 aren’t "just" weight loss drugs.

They have complex metabolic effects, including reducing whole body inflammation by acting on the brain, partly in a weight-loss independent manner.

GLP-1 receptor agonists, and related medications, can help people but can also be misused at a societal level.

Let me elaborate (link 🔗 at the end)...
#GLP1 #inflammation

2/4) In their best use case, the metabolic actions of GLP-1 can catalyze lifestyle change. For example, reducing “food noise” permits patients to make healthier choices when set in a modern food environment that is itself obese with UPFs, sugar and temptation.

3/4) However, at a societal level, we should be cautious not to forget that the root cause obesity is metabolic dysfunction caused by an unhealthy lifestyle.

Thus, the core solution is lifestyle, and it’s unlikely we will “pharma” our way out of the obesity epidemic. However…

I am NOT saying “people should just live healthier.” Rather, I am saying that – as a society – we should push for a reevaluation of social norms around food and reconstruction of the food environment.

This can be in parallel to innovations in pharmacotherapy, deployed in the “right” patients. The determination of who those people are is not a matter for public discourse, it’s a private matter between physician and patient.

So, for our part, we should keep pushing for a change in the food environment, dysfunctional norms, and help people live a metabolically healthy lifestyle.

Read 4 tweets

Nick Norwitz

@nicknorwitz

Jan 4

🧬💥What if I told you that social stress doesn’t just mess with your head—it damages your DNA and biologically ages you? (link at the end)

🧵1/9) That’s not hyperbole; it’s hard science from new data published in @NatureAging

If you’re like me—juggling a life full of psychological stress—you might be wondering: How can I fight back?

Let’s break down the data...

(I'll tease: this thread also includes a little honest opinionated "revealer" about @hubermanlab)

2/9) Background on Aging (Senescence and p16)

Aging is complex, and there’s no one easy way to measure biological age.

However, certain hallmarks of aging—like DNA damage, telomere shortening, and cellular senescence—are widely recognized.

“Senescence,” the process by which cells age and stop dividing, accumulates as we age and plays a role in chronic diseases like heart disease and Alzheimer’s.

While senescence has some adaptive functions, for our purposes, it’s fair to call it a hallmark of aging.

Senescence can be triggered by inflammation and DNA damage.

👉And senescence can be measured by markers, like “p16”. (If you want to remember this, just imagine the stress of having a pissed off 16 year old kid.)

3/9) Social Stress Increases Marker of Senescence

In this study the researchers subjected mice to chronic social stress or, more specifically, “chronic subordination stress”: The experimental mouse is exposed to an aggressive dominant mouse daily.

The human equivalent would be like a bully at school, an abusive parent, or a hyper-aggressive boss.

In just 4 weeks, the experimental mouse (the one that got bullied) exhibited increases in markers of senescence, predominantly p16.

And this marker of senescence and aging accumulated over time, with levels as high as 12X that of control mice by 26 months of age in circulating blood cells.

Read 9 tweets

Nick Norwitz

@nicknorwitz

Jan 2

Unexpected Benefits of Compound Found in Olives on Muscles 🫒💪(link at the end)

1/9) High Level: These new data show how a specific compound found in part of the olive plant can improve muscle performance in the short term, and potentially fight off age-related muscle loss.

I’m going to first break down the data, and then tell you how to use it for maximal muscle benefit

#Exercise #Muscle #healthyaging

2/9 But first, I’m going to need to review with you a bit about how muscles work at the molecular level.

PLEASE bear with me here, because it will be fundamental to our discussion of the data – as well as your general understanding of how muscles work.

Inside muscles, there are long filamentous overlapping proteins called "actin" and "myosin." The myosin has these little heads that branch off and grab on to actin.

When a nerve impulse hits a muscle, it causes a release of calcium inside the cell, and this allows myosin to walk along actin, pulling them together and increasing the overlap between actin and myosin, which translates to shortening of the muscle – a muscle flex.

That, in effect, is a muscle contraction.

💪🧀Now, here’s something important: this process is highly dependent on calcium.

It’s calcium that allows the actin and myosin to interact. And its calcium that also signals to the mitochondria to meet the energy demands of a muscular contraction.

🏎️Analogy: Calcium is to muscle as a responsible driver of is to a car. Calcium presses the gas pedal (signals muscle contraction) and fuels the tank to keep the engines (mitochondria) running.

3/9 Okay, now let’s introduce 1 of 3 key players: the mitochondrial calcium uniporter (MCU).

MCU is what transports calcium into mitochondria, and thus enables signaling to mitochondria to boost energy production.

(We will explain how it does so momentarily.)

And the MCU is partnered with another protein, our 2nd player, MCU regulator 1 (or MCUR1), which is MCU’s essential sidekick: Like Batman and Robin.

MCU and MCUR1 work together to let calcium into mitochondria, and this is essential for energy production.

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