Suzy

[Suzy @TweetSuzy]

@HalCranmer @janellison "Keto"

[Benjamin Bikman @BenBikmanPhD]

My lab just published a very neat case series. https://t.co/vuaF1t5YLg

We asked the question, working with clinicians: Can a low-dose GLP-1 RA (e.g., semaglutide, tirzepatide, etc.) coupled with a low-carbohydrate diet yield better results than the conventional high-dose use of GLP-1 RAs. The answer is a resounding "yes".

We found that over 90% of the weight lost with this personalized approach was directly from fat loss, with some even increasing their lean mass during active fat loss.

Of course, it's a case series and should be viewed as hypothesis generating, rather than definitive. But I think this is the best use of these drugs. They should not be viewed simply as "weight loss drugs", but rather "carb control drugs". They are a crutch to help people learn to control carb cravings. The dose should be low enough that the person still feels the cravings, or can acknowledge them, but decides not to indulge. This enables not only a lower dose, but also hints at an offramp. Over time, the person is ideally able to stop the drug, but with new habits.

Thanks to https://t.co/2PASwK6lc8 for the clinical assistance and @InsulinIQ for the coaching.

[Toku @TokuHealth]

@newstart_2024 The dose part is what most people miss. The study Sinclair references (PMID: 36072877) used 10,800 FU/day for 12 months in 1,062 participants + vitamin K2, which is what we formulated our product off of.

A lot of nattokinase products on the market are nowhere near that dose.

[Mirwais میرویس, MD @ultramed38]

The Chinese study is real and the results are striking but the dose detail matters enormously. At 3,600 FU/day (the standard supplement dose) the effect disappears entirely. The plaque regression only appeared at 10,800 FU/day, roughly 3–5x what most people are actually taking. The 3-year RCT at 2,000 FU found zero effect on carotid IMT. Interesting mechanism. The dosing question is unsettled. Worth watching but not worth assuming your standard capsule is doing what Sinclair is describing!

[Camus @newstart_2024]

@davidasinclair talked about nattokinase and plaque reversal in this conversation with @PeterDiamandis.

https://t.co/xvk6rLUYO4

[Camus @newstart_2024]

David Sinclair says he’s been reversing plaque in his arteries with nattokinase.

On Peter Diamandis’ podcast, Sinclair shared that he’s been taking it for years and mentioned a Chinese study with 1,086 people that showed up to 95% plaque reduction in one year at sufficient doses (at least 12 fibrinolytic units daily). He also checks his own carotid arteries with ultrasound and says there’s no buildup.

Nattokinase is an enzyme from fermented soybeans that breaks down fibrin. Some human studies show it can help reduce arterial plaque and improve blood flow, but results vary. Larger, high-quality trials are still limited, so it’s considered promising but not definitive.

Cardiovascular disease is still the #1 killer. If there are accessible tools that support artery health beyond statins and lifestyle, it’s worth paying attention.

Have you heard about nattokinase or tried anything similar for heart health?

[Be Believing @Be_Believing]

He wanted to gently make fun of the size of his wife's water bottle. 🤣🤣🤣

[Paul Mason MD @DrPaulMason]

All too often, there is a lack of nuance in discussions surrounding obesity and weigh loss. In this series of tweets, I address the core issues, while also touching on several important, yet overlooked topics. I suspect much of this content will be new to most conventionally trained doctors.

Understanding Obesity: The Role of Hormones and Nutrients

The Calories In/Out (Energy Balance) model of obesity is wrong

Imagine if you went to a doctor, and after assessing you, they said - ‘Of course you feel terrible, you have a fever of 40°C (104°F). All you need to do is bring down your fever and you’ll feel better’. Would you be happy? While this information is accurate enough, it is completely unhelpful, in that it doesn’t provide any advice at all on how to actually bring the fever down.

Patients attending doctors for assistance with weight loss often receive equally useless commentary. In line with the "calories in/calories out" model of obesity, they are simply told they need to expend more calories than they take in. The problem is, they are often not given any advice on exactly HOW to do this. And when they are given advice, it is often completely wrong. Many doctors advise patients to restrict fat intake, primarily on the basis that it is more energy dense than either protein or carbohydrate.

The problem is, the Calories in/Calories out energy balance model of obesity completely ignores the sciences of biochemistry and endocrinology, overlooking differing effects of fat, protein and carbohydrates on hormones. By oversimplifying the cause of obesity to a simple case of caloric balance, incorrectly presumed to be entirely under volitional control, obesity is thought to represent a failure of will power. In essence, the implication is that most obese individuals are lazy and overindulgent, something that is both manifestly false and an egregious form of medical gas-lighting. The truth is, low fat foods, which typically contain large amounts of carbohydrates, have been scientifically proven to cause weight gain.

It's not however, that doctors give poor advice maliciously. Many doctors after all, follow their own advice, which may explain why in 2015, nearly 60% of Australia’s doctors were overweight or obese.

Hormonal Influences on Weight Gain
Most people are aware that thyroid hormone helps to regulated our metabolism, and that deficiencies can result in weight gain. The fact is, there are at least a dozen hormones whose dysregulation has been associated with weight gain. For example, high cortisol levels as seen in Cushing’s syndrome may lead to distinctive fat deposits known as "moon face" and "buffalo hump." By far the most significant obesogenic hormone, however, is insulin.

Insulin and obesity
A 1996 study conducted in Bogalusa, Louisiana, highlighted the crucial role of insulin in obesity . Over an 8-year period, the study measured insulin levels in children and young adults. It found that those with the highest insulin levels (in the top 25% at both the beginning and end of the study) were 36 times more likely to become obese compared to those with the lowest insulin levels (in the bottom 25%). Specifically, the risk of becoming obese was just 2% for those with the lowest insulin levels, while it soared to 72% for those with the highest insulin levels.

Type 1 diabetics well know that fattening effect of insulin. Before they are diagnosed, and commence insulin therapy, many type 1 diabetics are dangerously underweight. The reality is that, without insulin, the body cannot store fat. The commencement of insulin therapy can rapidly reverse this emaciation, research showing that type 1 diabetics gain an average of 5.1kg (11.2lbs) during their first year of insulin therapy . Despite its life saving potential in type 1 diabetics, up to 60% of type 1 diabetics may deliberately reduce or skip insulin doses due to its fattening effect – a condition referred to as diabulimia .

Further evidence of insulin's fat-storing effects is the development of localised fat masses at sites of injection. Known as lipohypertrophy, this can occur in anyone who injects insulin, one study reporting that 49% of all insulin injecting type 2 diabetics developed lipohypertrophy . *

*Importantly, many adults diagnosed with type 2 diabetes may actually have an autoimmune form that impairs insulin production. This condition, known as Latent Autoimmune Diabetes in Adults (LADA), is present in about 10% of diagnosed type 2 diabetes cases. Individuals with LADA are often more slender than typical type 2 diabetics and may even be underweight. While a strict low-carb diet is generally beneficial for these individuals, insulin therapy is often necessary.

[Chief Nerd @TheChiefNerd]

New Jersey right now 🤣

[Dr. Matthew CL Phillips @drmclphillips]

This is a relatively balanced article about seed oils, we need more rational, balanced approaches to contentious issues:

https://t.co/Gi8Q2v0cjt

[Suzy @TweetSuzy]

Check out Megan Tibbits's video! #TikTok https://t.co/XwYEDr9kWN

[American Diabetes Society @OfficialADSOrg]

A ketogenic diet made of real, whole foods is a smart choice for people with diabetes. Here, is the @TheSMHP document with 300 citations for healthcare providers & patients. Doctors can use this to help their patients.
https://t.co/z56DzMbatZ

[HLTH CODE @gethlth]

Is Berberine a super supplement, or is it just hype? Let’s dig into the science.

@BrianLenzkes @BiggestComeback @TempleDietitian @BenBikmanPhD

https://t.co/X009YzUYaI

[Suzy @TweetSuzy]

@Fynnderella1 @CommunityNotes @elonmusk 7. Cg c. C cc. 87 uu uccc. Uu u u. Uu.

[Suzy @TweetSuzy]

See this Instagram video by @megantibbits https://t.co/I2EEUwATZp

[The Real Dr. Steven Horvitz @IMWHorvitz]

Cholesterol is a marker 
Insulin resistance is a mechanism

Markers don’t cause disease. 
Imbalanced mechanisms do

Medications that alter markers without affecting the imbalanced mechanism are not cures not treatments nor preventives. They mostly help your 401k if invested in #BigHarma

[Benjamin Bikman @BenBikmanPhD]

Saturated Fat has been the Boogeyman of Low-Carb for too long. This video by @nicknorwitz should put that myth to rest. You're going to want to bookmark this one! YouTube: https://t.co/8RuWzPgwYG
Also read/share: #OreoVsStatin
https://t.co/p9EF6W2nn1

[Benjamin Bikman @BenBikmanPhD]

I try not to be a drum-beating advocate of a ketogenic diet, but when it comes to neurological disorders, it increasingly appears as though some advocacy (and broadcasting) is warranted. This is a newly-published case study that documents the improvements in symptoms of a patient with ALS. Tragically, the patient suffers from a particularly devastating variant with a mortality of ~24 months. On his own, as the case report documents, the patient instituted a ketogenic diet. Clinicians reported "...he improved in ALS-related function (7% improvement from baseline), forced expiratory volume (17% improvement), forced vital capacity (13% improvement), depression (normalized), stress levels (normalized), and quality of life (19% improvement), particularly fatigue (23% improvement)." Not all clinical markers improved, but any improvement with this disease is remarkable. Even more remarkable is that the improvements have persisted, as they note "Now over 45 months since symptom onset, our patient remains functionally independent and dedicated to his TRKD." There is no doubt that the myriad cells of the nervous system respond favorably to ketones as a fuel source. https://t.co/nEPmuRifWV

[Dr. Vipul aggarwal @drvipulaggarwal]

So very true ....

[Suzy @TweetSuzy]

Fascinating! https://t.co/DF95UjfUkf