Anyone been reading Peter Attia?

I discovered him recently and was absolutely delighted that I'm not alone in thinking that obesity is a symptom of T2/insulin resistance and NOT the cause. There's some pretty bad science out there on those lines and it's become something "Everybody Knows" that obesity causes T2 and that PWD can lose weight and be less lazy and greedy and blameworthy. I'm looked at as some kind of an idiot when I suggest it. Sure they've shown a LINK, but not causality. I am not medically qualified, although I have a degree in a biological discipline[from 1970, when it was worth something!] and a very high IQ. Nevertheless nurses, who sometimes know NOTHING about biochemistry or metabolism, at least here in England. are aknowledged experts and I'm a mere eccentric.
thank you so much Dr. Attia!
Hana Rous

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I am not familiar with him however Brian posted Ralph Difronzo's name online and I looked him up and found an interesting article about recent research on T2 and how it plays out in the treatment arena which is the best one I've found. It's fairly science-heavy but seems to be very comprehensive:

I've watched several videos and also read his blog He's a medical Dr. so he knows biochemistry inside out.

A few years ago he found he was developing Metabolic Syndrome, often a precursor to T2. He was gaining weight despite being an athlete and eating the standard healthy athletic diet (high carb, high protein, low fat). His solution was to cut carbs drastically and raise his fat intake. He lost 40 lbs. and his symptoms of metabolic syndrome disappeared.

His latest project is the Nutritional Science Initiative which aims to fill in the holes in our knowledge of nutrition and get to the bottom of the current obesity/diabetes epidemic.

Here's a video previously shared by Judith, in an earlier post, that touches on the issues you raised, Hanna.

When people doubt me when I tell them about this, I explain it as follows:

The typical pattern for weight gain from excess insulin is around the middle. No one knows why, but it's true. So something else starts off weird--it could be extra insulin secretion or a problem with insulin receptors, but there's a problem there first. That causes the weight gain, which then causes more insulin resistance, which causes more weight gain, etc. It's a vicious cycle that's incredibly hard to break (especially because insulin makes you hungry).

It's interesting how, when it comes to weight and the medical community--especially in obesity--no one cares to look into correlation vs. causation. Obesity is correlated with T2, but no one ever proved that obesity causes it. If obesity did, in fact, cause T2, then nearly everyone who's extremely overweight should have it, not 1/3 of these people.

Most obese people don't get T2 and it tends to be a specific type of weight gain that could very likely be diabetes related, so there is a chicken and egg issue. Also, I've been thinking that since LADA type 1 diabetics (who slowly lose insulin production over years) have insulin resistance comparable to type 2 diabetics (seems to be nearly the same when BMI is taken into account), the insulin resistance is probably the result of decreased beta cell production, and not the other way around.

I think our sedentary lifestyle and easy access to carb laden foods probably play a role in the expression of T2 diabetes, but the underlying cause is probably more related to genetics and chemical exposure.

Insulin resistance is an inability of the body to efficiently use what it has. Decreased beta cell production is an inability to keep up with the demands.

The reason why only 1/3 of obese people get T2 is because the other 2/3 make up the deficit with insulin--they need more insulin to get over the insulin resistance, but they make it just fine and don't get high BG's.

People with LADA have insulin resistance and decreased beta cell mass, just like the 1/3 with T2. I'd love to hear where you heard that their insulin resistance levels are similar after adjusting for BMI, because I've never heard that before.

I agree about the sedentary lifestyle/carbs and genetics issue. I tell people about that all the time, too!

I have less than <.05 c-pep I have tested positive once for antibody's and my insulin requirements will more than double with just a 25 lb increase in BMI so my body weight has a huge impact on my insulin requirements. At my recommended BMI of 172 lbs my TDD is 45u and at 195lbs it is 100u.

My TDD is normal for a T1 that is 5'-11' and 172 lbs but if I add 20 to 25 lbs to my BMI then my body needs 100% more bolus insulin to deal with the same amount of carbs, my basal only goes up about 20%.

More scientific a proof is that if obesity causes T2, there CANNOT be any slender lightweight T2s and we know there ARE lots of them.
Koch's postulates, which are a test for causality [of infection] state that ALL cases MUST have the presence of the suspect infectious organism.
I paraphrase. It's over 40 years since I learned this and haven't looked it up.

I have recently "discovered" and regularly read his blog The Eating Academy. I was trained as a scientist and it is a relief to find people like Dr. Attia. For years I wondered about the paradox of so many fat people in so many different cultures/situations. He has an intellectual humility that is refreshing and the science in his posts is accessible to many. He presents his ideas as hypotheses which is the essence of scientific methodology.

He is associated with Gary Taubes (Good Calories, Bad Calories). Reading that book will undermine your confidence in the "experts" and conventional "wisdom." As an example, just took a quiz on SparkPeople about diabetes and they had two question answers wrong regarding the role of fats.

Insulin resistance is when the cells are less responsive/sensitive to insulin. Decreased beta cell production can result from the beta cells being killed off (immune system attack, chemical exposure, or being overstressed) OR from an inability to keep up with demand.

Again, the issue is: which came first (decreased insulin production or insulin resistance) and what was the mechanism that triggered it. Correlation is not causation, and while many T2s are overweight and that weight plays a role, being overweight may not have triggered the disease and may largely be a symptom.

So again, the insulin resistance could very well be the result of a decrease in beta cell production, and that would explain why insulin resistance also exists in LADA/T1 diabetics in a manner almost identical to that of T2 diabetics. LADA is late onset type 1 diabetes, and the difference between it and T1 in children is that its progression is slower (likely due to immune system differences). It does beg the question, why do the LADA people who are having an immune system response to beta cells (and are often think) also have insulin resistance? Maybe simply running high BG levels without enough insulin was the primary cause of the insulin resistance, and it (or something else) triggered the midsection weight gain.

As for the BMI....

Anyway, the traditional model may be wrong and I think more study is warranted.

Also read Kuhn's Structure of Scientific Revolutions.

Wow! I read that as an undergraduate in an elective called "The History of Science" in 1968. My advisor was a Nobel Laureate (scary smart)and he absolutely agreed with Kuhn. So I can see why you like Dr. Attia. Obesity research is dealing with a lot of data and an inadequate model currently.

I have read his blog for over a year. His explanation of cholesterol was excellent, something every doctor should read, as well as every diabetic who is routinely prescribed cholesterol medication. I have learned a LOT reading Dr. Attia. I appreciate his dedication and attitude as well as his knowledge.

"He has an intellectual humility that is refreshing and the science in his posts is accessible to many. He presents his ideas as hypotheses which is the essence of scientific methodology."

I couldn't agree more, beechbeard, this is what I really like about Attia. He has extensive anecdotal evidence from his own experience and he hypothesizes about why this might be because of his medical/biochemical knowledge, but he wants to test his hypotheses. This is what the scientific method is all about. I still have trouble figuring out why the medical/nutritional establishment recommendations are based on such thin experimental proof, and why they reject experiments that go against what they "know" to be true.

When he talks about his Nutritional Science Initiative he points out that there is a diversity of opinions within the organization, very much on purpose. This is the most efficient way to arrive at the truth.

Hypothesize, test, re-hypothesize, test............

You didn't provide a link to anything written by Attia, and I have never heard of and therefore never read anything by him. Please provide a link if you can.

As for the LINK between T2 and obesity, it is fair to say that the only conclusion that can be drawn from that observation ALONE is that there is a correlation, and the direction of causation is not clear. But I think there are some other studies that DO provide better evidence that there is in fact a causative link from excess weight leading to T2 diabetes, and not the other way around as you are suggesting.

One of these would seem to be the Pima Indian studies. Back before the Pima indians ate the SAD (standard american diet) diet rich in calories from saturated fats and refined carbohydrates, they also got a lot of exercise doing subsistence farming. They burned off the high fiber diet they ate and had normal BMI - and they also had essentially no T2 diabetes.

After their land was stolen and they were put on reservations, their diet and exercise changed dramatically and they gained weight and BMI. They also developed a very high incidence of T2 diabetes. Crucially, their genes did not change - and there is clearly a genetic component involved (as there is in most or all T2 diabetes).

But their genes did not lead to T2 diabetes as long as their diet and exercise were balanced to keep them from becoming overweight. It was only after their diet was changed and their exercise was dramatically reduced that their BMI and incidence of T2 diabetes skyrocketed.

this is incorrect. LADA, is type 1, that's all it is..and, not ever child presents in DKA, they too can have a very slow onset, can be caught early, have a honeymoon, so the 'term' LADA is useless. Type 1's don't have insulin resistance, it's one of the diagnosis tools used to determine type 1 and type 2. beta cell destruction is characteristic of type 1, i.e., type 1's make no insulin, and other hormones, alpha cells are destroyed in the process, too. beta cell destruction has nothing to do with insulin resistance. i have no beta cells left because I am positive for the autoimmune disease, the 'antibodies' which kill off the islet cells. but I am insulin sensitive to insulin, as are most type 1's. insulin resistance means one's body makes enough insuln (type 2's who have beta cells and are not defficient of insulin) but they're resistant to their own insulin production because, usually, due to excessive weight. that's what causes insulin resistance. the body cannot use it's natural production of insulin. type 1's make NO insulin!

I think the study that Scott A may be referring to is Palmer et al (2005), "Is Latent Autoimmune Diabetes in Adults Distinct From Type 1 Diabetes or Just Type 1 Diabetes at an Older Age?" The findings of that study seem to say that obese LADAs have comparable insulin resistance to Type 2s, not that all LADAs have comparable insulin resistance to Type 2s. Also, the Palmer study did not compare insulin resistance in obese rabid onset Type 1s to obese LADAs and Type 2s, but of course Type 1s can develop insulin resistance. Just anecdotal, but most LADAs who post here on TuD seem to be insulin sensitive.

Interestingly, today there is still a group of Pima Indians in Mexico who live the traditional lifestyle. They have very low rates of obesity and very low rates of Type 2 diabetes.

His blog is a good place to read some of his writings.

Here's the Ted talk link the Judith refers to. I watched it the first time she posted it. Very impressive.