Nutrition & Chronic Disease Researcher | Creating Content About Nutrition and the Prevention of Chronic Disease | Founder & Director @ Nourished by Science
I am excited to announce the launch of Nourished by Science, a new website and YouTube channel dedicated to the highest standards of scientific rigor in communications about the links between nutrition, health, and chronic disease.
In the 1970s the dietary guidelines in the US started recommending a low-fat, high-carb diet.
One argument often made is that the resulting increase in carb consumption triggered the obesity epidemic.
Lipids such as triglycerides or cholesterol need to be packaged for transport in the blood.
These transport vehicles are called lipoproteins.
There is a lot of confusion about the different types of lipoproteins, so let's discuss the basics of lipoprotein metabolism.
🧵
Lowering LDL-cholesterol reduces the ABSOLUTE risk for a CVD event only minimally.
From this fact, some people conclude that LDL-cholesterol is not an important risk factor for atherosclerotic CVD.
IMO, that conclusion is poorly conceived.
Many authors of social media posts and even nutrition books seem to think that "evidence-based" means that you can make the statement "X causes Y" as long as you can cite one paper to support that statement.
What this leads to is a situation like this:
@MicrobiomDigest
The one thing I object to is doing tons of reviews and editorial board duties for free, and then getting charged $2,000 in publication fees by those same journals for my own papers, some of which I have to cover out of pocket. Something about this feels very wrong.
A common claim online is that only small, dense LDL particles are atherogenic, and that large, buoyant, or "fluffy", LDL particles can safely be ignored.
What is all of that about?
What does the scientific evidence say?
A 🧵
#ldl
#ASCVD
#CVD
#atherosclerosis
#lipoproteins
There is a common narrative on social media that lower blood sugar levels are always better, and that sugar spikes after a meal should be avoided like the devil.
@realDaveFeldman
@BudoffMd
Super interesting. It's early days, and a small cohort, but I feel that this line of work promises to teach us something new about the relationship between LDL-cholesterol/apo B-containing particles and ASCVD.
Even though it's just the baseline data, given that participants
A new video is out wrapping up our discussion of the link between ultra-processed foods, overeating, and the obesity epidemic. Features an RCT by
@KevinH_PhD
, and practical tips we can learn from this work to minimize overeating.
via
@YouTube
Energy density is a crucial factor that is often not given enough attention despite having a significant impact on ad libitum energy intake.
Energy density is simply the calorie content of a food, meal, or diet per g (or per 100g).
On the population level, the body mass index and body fat mass are strongly associated with insulin resistance and an increased risk of type 2 diabetes.
For example, the graph below is based on data from the Nurses' Health Study:
Recently, several influencers on X tweeted about an RCT in which patients with fatty liver disease were randomized to consume a diet rich in fruit or low in fruit.
Let's discuss the results and consider them in the context of the broader literature.
New video: The nutrition transition towards an industrialized food system rich in ultra-processed foods has coincided almost perfectly with the obesity epidemic in populations around the world. Summary of the data, and my thoughts:
When we gain weight, our body needs to store extra fat. This could be stored in different tissues:
In subcutaneous fat (just underneath the skin).
In visceral fat (surrounding the inner organs).
In ectopic depots (tissues such as liver and muscle not designed for fat storage).
A THREAD about FRUCTOSE and SUGAR-SWEETENED BEVERAGES:
If we drink a beverage sweetened with high-fructose corn syrup (i.e., 45% glucose, 55% fructose), the fructose concentration in our peripheral blood stays very low.
About 90% lower than blood glucose levels.
Why is that?
Recently, the excellent Nicola Guess
@Dr__Guess
wrote up her thoughts about blood sugar spikes and CGM use.
I tend to agree with Nicola on most points, but there is one key point in which our interpretation of the scientific evidence differs.
A friendly rebuttal ...
@NikosNoulezas
@LDLSkeptic
David, I have read all of your published papers related to LDL-chol and watched several of your presentations, and, respectfully, I don't find your argument convincing.
And I am saying this even though I do agree with you that the evidence that LDL (or apo B-carrying particles)
New YouTube video: Do Carbs Cause Insulin Resistance?
In the newest video, I am taking a thorough look at the scientific evidence to shed light on whether insulin sensitivity differs between low-carb and high-carb diets:
New video:
Causes of Insulin Resistance: The Personal Fat Threshold Hypothesis
Discusses a key concept linking excess body fat mass to insulin resistance, glucose intolerance, and type 2 diabetes.
AJCN just published the main paper of the dissertation project of
@kelseyaschmidt
, a randomized controlled trial of the impact of low-fat or full-fat dairy foods on glucose homeostasis.
@realDaveFeldman
@BudoffMd
Yes, the data have affected what I am going to share in the video. I had planned a section discussing common claims that LDL-chol/apo B are not important risk factors for ASCVD. One of these claims was that high LDL-cholesterol on ketogenic diets is not atherogenic. So far, this
Postdoc Opportunity in Clinical Nutrition Research! We have a fundable score on an R01 to study the acute effects of overfeeding on hypothalamic gliosis (in humans, as measured by MRI). PI and primary mentor would be Ellen Schur at the University of Washington.
Important point made here by
@Paddy_Barrett
.
I made a similar point in my recent video, linked below. Critics of the lipid-heart hypothesis often point out that the ABSOLUTE risk reduction in lipid-lowering trials is small. While this is factually correct, it is a poorly
Most people overestimate their risk of heart disease in the near term
And underestimate their risk over the long term.
Here is how to calculate Lifetime - Risk & Benefit
📕 Make Sure To Bookmark ✅
/1
Particularly if we look globally, we see a correlation emerging between the consumption of UPFs and obesity prevalence. Specifically, obesity rates have remained low in high-carb countries such as Italy that have - so far - not adopted UPFs widely.
I really like this editorial by
@lowcarbGP
One problem in diabetes & nutrition research these days is that ambitious larger-scale RCTs that investigate diet and lifestyle change for the reversal, as opposed to the management, of T2DM are usually not fundable because they are
1/3 Published today my first ever editorial 😊Are we getting good value from all the money spent on research into nutrition and obesity ?? Obesity rates are climbing ++so perhaps not. I suggest an alternative
Maybe eating more refined carbs and sugars played a role, but we may want to consider the other tremendous changes that have occurred since the 1970s in the US (and global) food system, particularly the move towards ultra-processed food (UPF).
Many commenters on my YouTube videos think that developing insulin resistance takes many years or decades.
This is not necessarily the case.
In fact, specific triggers can cause insulin resistance in minutes to hours.
It depends on which trigger we are exposed to ...
@drpablocorral
@US_FDA
@EMA_News
I think you misunderstand the design of the study. Participants were not enrolled in a keto diet, but were free-living people following a keto diet who happened to have a phenotype characterized by isolated massively elevated LDL-cholesterol. It's an observational cohort, and
UPFs are "industrial formulations of foods with typically 5 or more and usually many ingredients". They usually contain sugar or high-fructose corn syrup, added oils and fats, and a long list of "substances not commonly used in culinary preparations".
I am not saying that the global obesity epidemic can be entirely attributed to UPFs.
In fact, the whole point of this thread is to suggest that the obesity epidemic almost certainly does not have a single cause.
A better way to think about this conceptually is that if we minimize exposure to all CVD risk factors, the sum of several small absolute risk reductions in the short term should amount to a very meaningful absolute risk reduction in the long term.
That is what we are aiming for.
@NutritionMadeS3
Thanks for sharing, Gil. That's a great find, and I really enjoyed reading it.
The primary exposure here, the corrected insulin response (CIR) is a measure of the early insulin response, relative to the early increase in blood glucose. The early insulin response (first 30
Highly recommend this new video by Gil, even if you are not interested in the particular influencer named in the title. This is a very important, and well presented, discussion of some of the key problems in science communication on social media and in nutrition books.
Gil
High-carb foods such as grains and potatoes are staples of most people's diets.
However, some people are concerned that eating these foods could give them a blood sugar spike.
Here are 6 evidence-based strategies to avoid a blood sugar spike when eating a high-carb meal.
However, I suggest we are careful with oversimplified statements that blame the carbs for everything the UPFs, and likely numerous other dietary factors, at least contributed to.
If we consider the time since 2000, however, when obesity prevalence has again almost doubled, there has been no significant change in the relative proportion of calories eaten as carbs vs. fat.
See Fig 1 in this paper here:
If we compare low-UPF diets either high or low in carbs, as in DIETFITS, we find that both lead to similar weight loss.
This is inconsistent with the idea that the carb content of the diet is the primary determinant of energy intake and body weight.
@drpablocorral
@US_FDA
@EMA_News
@drpablocorral
, no, I understand this concept very well, and my response to you was not to question the relevance of apo-B-carrying particles for ASCVD.
My point was an ethical one: if people freely choose to adopt a ketogenic diet, for - on average - 4+ years, and obviously
"I must have watched literally 100s of nutrition and health videos over the last 5 years and this is without doubt the absolute BEST. Clear, well explained with no food tribe drama. [...]"
Comment on this YouTube video:
Among healthy people with normal glucose tolerance who have blood sugar in the 70-140 mg/dL range much of the day, however, there is little evidence that they benefit from 'optimizing' their blood sugar levels further. Any potential benefit in that group is also likely small.
New video and blog post out:
The Regulation of Blood Sugar!
We cover:
- How our bodies regulate our blood sugar levels
- What goes wrong in these processes if we develop diabetes
- How to interpret lab results related to blood sugar
- How diabetes is diagnosed
Continuous glucose monitors, or CGMs, have traditionally been used by people with diabetes, but have recently also become popular among healthy people with normal glucose tolerance.
A new nutrition book has just been reviewed by
@redpenreviews
!
Of the books we have reviewed so far, this is the highest-scoring book that recommends a low-carb diet.
The primary reviewer was the very talented
@SamuelDickenUK
That Nature Medicine paper claiming to link dietary erythritol to cardiovascular events!
A lot has been said and written about it, but I still feel compelled to share some thoughts.
A thread about why the paper should not have been published like this.
Fourth, I suggest we often think about chronic disease risk factors incorrectly.
The risk of a CVD event is not determined by the current exposure to that risk factor (i.e., our LDL-cholesterol level today), but by our cumulative lifetime exposure to the risk factor.
Citing 1-2 papers that support our claim while not considering or mentioning those that don't is almost as bad as simply making up stuff.
Maybe even worse, because citing papers gives the appearance that a claim is based on evidence.
That's a wrap!
If you enjoyed this:
1. Follow me for more content on nutrition as it relates to the prevention of chronic disease.
2. Like and/or share this with your audience.
In the 1970s the dietary guidelines in the US started recommending a low-fat, high-carb diet.
One argument often made is that the resulting increase in carb consumption triggered the obesity epidemic.
New blog post and video:
"How to avoid blood sugar spikes, without reducing carbohydrate intake."
Covers six evidence-based strategies that reduce the postprandial increase in blood sugar levels after eating.
Are you clear on how to interpret lab data related to blood sugar regulation, such as fasting glucose, HbA1c, or data from an oral glucose tolerance test?
If not, this video here will answer all of your questions:
That then raises the question whether we are losing weight on low-carb diets because we cut out the carbs, or because we cut out all of the ultra-processed junk foods?
When we are young, almost all of us have very low blood cholesterol, triglyceride, and glucose levels, and low blood pressure.
Once we cross into our 40s, 50s, and particularly 60s, most of us notice that all of these values have gradually crept upward.
Third, atherosclerosis is a multi-factorial disease that takes decades to develop.
It is unreasonable to expect that addressing only one CVD risk factor for a few years will reduce the CVD risk to zero.
Help!
For my new video and blog post, I am researching factors that increase ad libitum energy intake.
I was curious whether diets that elicit greater glycemic and insulinemic responses increase energy intake in the short term (within a meal or two, within a day, or a few
New video alert: "A Metabolic Double Whammy: Liquid Calories"
Covers the impact of alcoholic and sugar-sweetened beverages on calorie intake, body weight, and liver fat content.
The argument I'd like to make is that the relative changes in carb and fat intake were almost certainly too small to explain the substantial increase in obesity prevalence.
In contrast, HDL particles are released by the liver and the GI-tract as a protein, not a full lipoprotein.
While VLDL sheds lipids in the blood, HDL particles bind and accumulate lipids while circulating in the blood.
A single cause is unlikely because dietary factors don't exist in isolation: UPFs, for example, contain refined carbs as a key ingredient by definition.
So, when people started eating more UPFs, they also ate more refined carbs.
Vice versa, any low-carb diet is low in UPFs.
Just published a new video to answer the 7 most common viewer questions about blood sugar spikes.
This video includes a detailed explanation of how I define blood sugar spikes, and why such spikes may be linked to an increased risk of chronic disease.
VLDL particles are released by the liver.
In the blood, VLDL particles shed triglycerides as they pass through tissues. The particle shrinks and becomes denser, it becomes IDL, then LDL.
Thus, VLDL, IDL, and LDL are the same particle at different stages in their life cycle.
Second, because a typical lipid-lowering trial has a short duration of only 3-6 years, the CVD incidence is low and usually in the single digits, even in the untreated controls.
As a result, the absolute risk reduction cannot even theoretically be an impressively high number.
Fasting apo B is considered the best blood lipid measure of CVD risk, followed by non-HDL-cholesterol and LDL-cholesterol.
Because Lp(a) is particularly atherogenic, it is often recommended to measure serum Lp(a) once in a lifetime to gauge the overall risk of CVD.
WOW!
Great new video by
@PlantChompers
on the nutrition book landscape in the US.
Strongly recommended, because it has an important message, and is fun to watch! Well done, Chris!
The lipoproteins differ in their ratio of protein to lipids, with HDL having the most protein and VLDL having the least.
Because protein (>1.3 g/mL) is a lot denser than lipids (<1.0 g/mL), the density of a lipoprotein increases with increasing protein content.
New video alert:
A Neglected Risk Factor for Chronic Disease: The Insulin Resistance Syndrome
Also available as blog post, including all of the references:
The point of this thread is not to argue against low-carb diets.
It is clear that well-planned low-carb diets can be health-promoting, and that many people have benefitted from them tremendously.
100% agree with Gil here.
There may be a lot of nonsense on YouTube, but creating a world with just a few gatekeepers who control what is and is not credible is very problematic in its own right.
YouTube's health misinformation policies are extensive.
Many ideas around COVID, vaccines, ivermectin, herd immunity and cancer treatment are essentially banned.
Reading this list sends a chill down my spine.
@robertlufkinmd
Both of these views are superficial half-truths. T2DM is primarily an issue of caloric excess (from any macronutrient) that cannot safely be stored in subcutaneous fat tissue.
Comparing diets high or low in UPFs with the same carb content, people eat way more calories on the high-UPF diet.
Again, inconsistent with the idea that the carb content of the diet is the primary determinant of energy intake and body weight.
Yesterday, I posted a poll about whether hyperinsulinemia causes insulin resistance.
I recently reviewed the data from hyperinsulinemic-euglycemic clamp studies and patients with insulinoma to understand whether chronically elevated blood insulin triggers insulin resistance.
Have been listening to an 8-part series on the scientific reproducibility crisis on the Healthcare Triage podcast. There is so much in there that resonates deeply. Excellent job by
@aaronecarroll
and team. Thank you for making this!
"The persistent finding is that it's not as credible, the published literature, as we might think it is or as we might hope it would be."
Have you listened to episode one of our podcast series on the reproducibility crisis?
#academictwitter
#science
The fact that we can still detect a clinical benefit of lipid-lowering therapy despite the small difference in the cumulative exposure between treated vs. placebo participants speaks volumes as to the importance of apo B particles/LDL-cholesterol in atherosclerosis and CVD risk.
New video and blog post: the measurement of insulin resistance.
I am discussing:
- why we may want to know whether we are insulin resistant,
- who may want to get tested,
- which test is recommended, and
- how to interpret lab results.
Lipoproteins also differ in their lipid composition, with VLDL consisting mostly of triglycerides, while the lipids in LDL and HDL are mostly cholesterol.
And lipoproteins differ by size, with VLDL particles having a 6-20 times larger diameter than HDL particles.
First, any investigator is under the ethical obligation to stop a trial and offer treatment to participants randomized to the placebo group as soon as there is statistical evidence for an a priori-defined clinical benefit.
That's why these trials are usually short (3-6 years).
Definitely worthy of a first tweet: honored to be part of the team at where we will try to sort out what is and is not based on scientific evidence in popular health and nutrition books.
Today, I'm excited to launch a top secret project I've been working on for the last year: Red Pen Reviews. Simply stated, Red Pen Reviews produces the most informative, consistent, and unbiased popular health/nutrition book reviews available.
I recommend this video by
@NutritionMadeS3
, in which he interviews
@Lipoprotein
to discuss the multifactorial nature of atherosclerosis and CVD.
With a particular focus on whether insulin resistance and elevated apo B are independent CVD risk factors.
@thefoolisingh
I recently received a very critical comment on YouTube by a viewer who complained that with the other influencers, you get a clear message, whereas with me there are too many words such as ‘suggest’ or ‘likely’ or ‘inconclusive’ or ‘limitation’ or ‘qualifier’.
These lipoprotein classes are not totally distinct particles; instead, they span the entire range in terms of composition, density, and size.
That is because lipoproteins constantly change in the blood by shedding or accepting lipids and proteins.
New video: a conversation with
@PenelopeFigtree
, an Australian MD, whose use of a CGM revealed that her blood sugar spikes in response to some supposedly 'healthy' foods, and that these spikes are frequently followed by reactive hypoglycemia.
All apo B-carrying lipoproteins are considered atherogenic.
These include VLDL, IDL, LDL, and Lp(a).
Because each of these has exactly one copy of apo B, we can assess the number of all atherogenic lipoproteins by measuring the concentration of apo B in fasting blood.
An idea for a new LMHR project:
Characterize the 24-h-DIURNAL variations in apo B/LDL-chol in LMHRs consuming a ketogenic diet vs. controls not in ketosis consuming normal mixed macronutrient meals.
Hypothesis: the reduction in apo B/LDL-chol in the postprandial period is more
Really appreciate this video here by
@NutritionMadeS3
, particularly for explaining very well how to think about the scientific process and the concept of uncertainty in science. Well done, Gil!
For example, the difference in the cumulative lifetime exposure to LDL-cholesterol between someone who has been treated with a lipid-lowering medication starting at age 60 (green) vs. placebo (red) is initially small (green-shaded area +/- yellow-shaded area).
New video and blog post:
The Dietary Glycemic Index: Everything You Need to Know.
Covers the glycemic index and glycemic load of common foods and explains how they are calculated.
When following the public discourse about nutrition and health, one can get the impression that few foods are safe for human consumption. Allegedly, carbs give us obesity and T2DM, fats lead to heart disease, and protein to cancer. 1/4