Lindsay Venn PA-C, RDLD, MHP

Passionate provider, focus on lifestyle, Bioidentical hormones, optimization, health span goals.

[Lindsay Venn PA-C, RDLD, MHP @linz1515]

@BrianLenzkes Love it!

[Benjamin Bikman @BenBikmanPhD]

GLP-1 medications are powerful and need to be used responsibly. I strongly believe they should be used at a lower dose and cycled with the purpose of learning to control carbohydrate cravings. Remember, like with every drug, there's a diminishing returns, when the drug becomes increasingly less effective if a high dose is maintained. Have an "off ramp", where a person can see test whether they've learned new habits and overcome the cravings for carbs.

[Benjamin Bikman @BenBikmanPhD]

I've been studying and compiling material for an upcoming Metabolic Classroom podcast on ivermectin and its metabolic effects. The more I learn, the more curious I am about the reasons why it's been so blacklisted.

Is it simply because it's used in animals? Well, so is metformin. So is aspirin. And many more. Why aren't those drugs equally vilified?

Remember, it's a Nobel Prize-winning drug for its effects on human health, and it shows profound impacts on mitochondria, cancer cells, inflammation, and even some evidence on insulin resistance.

Seems crazy not to continue to explore this drug and its potential application in, among many other things, cardiometabolic health.

[InsulinIQ @InsulinIQ]

Peptides are everywhere right now, but they’re not where you should start.

Get your metabolic health checked first. Then decide if peptides make sense.

Schedule a medical consultation with Lindsay here: https://t.co/DEoB8MKDTF

[Benjamin Bikman @BenBikmanPhD]

This is what worries me. What good is it to introduce more nutrition education in medical schools if the education is the same nonsense as before?

[Lindsay Venn PA-C, RDLD, MHP @linz1515]

@BrianLenzkes You speak the truth!!!❤️

[Lindsay Venn PA-C, RDLD, MHP @linz1515]

@BrianLenzkes 😢🙏

[Lindsay Venn PA-C, RDLD, MHP @linz1515]

Message me for the link!

[InsulinIQ @InsulinIQ]

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[InsulinIQ @InsulinIQ]

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[Benjamin Bikman @BenBikmanPhD]

One of thyroid hormones functions (among many) is to facilitate glucose uptake into cells. I wonder how many people have a "relative hypothyroidism" because their thyroid gland can't keep up with their glucose consumption?

[Benjamin Bikman @BenBikmanPhD]

Reminder: In the body, there is no insulin resistance without elevated insulin.

Whether it’s cause (more often than not) or consequence, elevated insulin will always accompany insulin resistance.

[Benjamin Bikman @BenBikmanPhD]

It's true! Our glucose-centric paradigm (i.e., lower glucose at all costs) comes with terrible consequences. An insulin-centric paradigm to Type 2 Diabetes is essential to actually solve the problem.

[Benjamin Bikman @BenBikmanPhD]

Have you been told you should worry about your thyroid with a ketogenic diet? Did you know that the more you eat carbohydrates, the more thyroid hormone you need to help with glucose metabolism?

Thyroid hormones, like T3 and T4, are vital for this process--they promote glucose uptake in tissues and regulate gluconeogenesis in the liver. However, on a low-carb diet with minimal glucose intake, the body requires less of these hormones to manage glucose metabolism. This reduction isn't a sign of thyroid gland deficiency; it's an efficient adaptation to lower carbohydrate demands.

Consider the parallel with insulin: On a high-carb diet, insulin levels rise to handle frequent glucose spikes. Switching to low-carb naturally lowers insulin because there's less glucose to process, which we correctly celebrate as improved insulin sensitivity and less need--not pancreatic dysfunction. The same logic applies here: declining thyroid hormones reflect a reduced need and optimized response to the diet, not a hormonal failure.

[Dave Feldman @realDaveFeldman]

Wow — 30k views since this morning.

Much 🙏 to everyone following our research and sharing the conversation.

[Benjamin Bikman @BenBikmanPhD]

Thanks for having me on as a guest. This was a great discussion.

[Peterson Academy @petersonacademy]

The relationship between cholesterol and mortality rates.

From @benbikmanphd's second course: Why We Get Sick.

[Benjamin Bikman @BenBikmanPhD]

I'm delighted to be back in Singapore, and I'm looking forward to my talk at the @NUSingapore @NUSMedicine. As I collect my thoughts for my upcoming talk, I am again fascinated by the differences in physiology and metabolic risk across ethnicities.

One thing really stands out: East Asians have a low fat threshold. In other words, a little fat goes a long way in creating problem.

Body fat is often vilified, but that's because we misunderstand its role in metabolic health. The mass of fat we store is less important than the size of the fat cells.

Europeans (as an easy point of comparison based on studies) have a higher propensity to make subcutaneous ("beneath the skin") fat cells compared with East Asians. Because of this, Europeans will tend to have more fat in general. However, the fat cells are smaller because there are more of them.

An East Asian, in contrast, tends to have fewer subcutaneous fat cells. Again, this seems like a good thing, and while it certainly leads to a body with lower total fat, with fewer fat cells to carry the metabolic burden, each fat cell is significantly larger. Moreover, with less subcutaneous fat comes a tendency for greater visceral fat (the main problem with visceral fat cells is that they grow more readily).

When fat cells get too large, they undergo two harmful changes: 1. They become insulin resistant to try to prevent further growth, and; 2. They become pro-inflammatory in an effort to stimulate new blood vessels (to provide oxygen to the growing fat cells).

All of this helps explain the unexpected phenomenon that while the average Singaporean is much leaner than the average White American, the rate of type 2 diabetes (a strong sign of insulin resistance) is higher in Singapore.

[Benjamin Bikman @BenBikmanPhD]

One of the more relevant aspects of understanding the long-term effects of what we eat on obesity and weight loss is the degree to which a free-living person (i.e., not a study subject) is hungry. As a result, studies that measure hunger responses to food are highly relevant, what is sometimes referred to as "return to hunger".

In this regard, dietary fats and carbohydrates don't have the same effect. As noted in this report (https://t.co/Dk0LYlckMM), and several others, "Participants consuming the [low-carb] meal reported lower appetite 3 and 4 hours following the meal, a response that was associated with the timing of the highest and lowest recorded glucose."

In other words, control carbs to control hunger. If the calories you eat make you want more calories, then it's not going to work out well long term.