Does a high-fat diet increase your risk of cardiovascular disease if you are diabetic?

By Lucia Fernandez Segura

In most cases, the prescription of a low-carbohydrate high-fat diet for patients with type 2 diabetes would be recommended. It is possible to justify such a recommendation by looking at the history of dietary recommendations for T2DM and the effects of LCHF on all the markers of T2DM and insulin resistance as well as looking for the vera causa of coronary artery disease.

As related in his investigative work, Rethinking Diabetes, by the science and health journalist, Gary Taubes: “Until 1913, specialists generally believed that copious dietary fat was a necessity in the diabetic patient”(1). In the origins of the discovery of diabetes (what we know as type 1 diabetes nowadays), the patients, frequently children or early teenagers, showed up to the hospital completely emaciated and about to die, incapable of utilising any of the energy provided by the intake of carbohydrates, no matter how many they ate, due to the incapacity of the pancreas to produce insulin (something that would be discovered many years after). Later on, a different type of diabetes would be discovered where the patients wouldn’t show symptoms of malnutrition but would develop severe accumulation of fat, excessive thirst, fatigue, polyuria, tissue damage, and several other health issues. It wouldn’t be until insulin was discovered and isolated that diabetologists would be able to identify the cause of type 2 diabetes, namely, insulin resistance, although, to this date, the medical profession continues to look at glucose without paying any or very little attention to insulin (1).

Before the creation of insulin therapy, both type 1 and type 2 diabetic patients were mainly treated with lifestyle interventions that varied between LCHF, very low calorie and other stretches of nutrition. In many cases, one of the reasons to determine the success of such interventions was the capacity of the patient to follow the recommendations for sustained periods of time. For decades, positive results were achieved with the prescription of LCHF diets, commonly animal-based (from 1797 by John Rollo to the early 1930s by E. Joslin and beyond) (1).

The creation of insulin therapy was the door for healthcare professionals to allow their patients to eat ad libitum and control their hyperglycemia with sufficient insulin dosage; even more so, in many cases, as they were learning to dose exogenous insulin correctly, the recommendations turned into an encouragement to increase the carbohydrate intake to make up for the excessive insulin dosage that would’ve caused a fatal hypoglycemic event (1).

The adoption of low-fat diet guidelines by the American Heart Association, originally based on the deficient studies of Ancel Keys, and later on by the American Diabetes Association during the second half of the 20th century led to the equivocal conclusion that, in order to improve T2DM, the majority of medical professionals would’ve suggested their patients to attempt many things but never to eat more fat, specially saturated, unless they wanted to suffer a cardiovascular event due to high blood cholesterol levels. Of course, if the energy intake of a person can’t in any way come from fat, it has to come, inevitably, from carbohydrates. This way of prescribing both lifestyle interventions and medication will continue for the majority of T2DM until our present time (1,2).

Over the years, several have been the attempts to prove that high serum cholesterol levels (and later on high LDL-c levels) were the cause of coronary artery disease or cardiovascular disease.

The studies that have found association between high LDL-c and CHD are rooted in the discovery of deposits of LDL-c in the atheroma plaque of a vascular lesion but, even to this day, the mechanism by which LDL-c is found there hasn’t been fully understood (3,4),  with some studies supporting the idea that the presence of LDL-c in the artery walls could actually be protective (5).

That high levels of cholesterol or high levels of LDL-c are the vera causa of CHD has never been proven (6,7) and in fact several studies have looked at the role of other lipoproteins as better predictors of CHD (8,9). The principle of vera causa applied to this hypothesis is that, for high LDL-c to be the real cause of CHD, the levels of LDL-c of all people suffering from the disease should be high but also that, in the absence of high levels of LDL-c the disease should not occur at all. Both scenarios have been refuted and hence the hypothesis should be considered incorrect (6,10).

However, there are promising studies that support the idea that insulin resistance could be the cause of atherosclerosis, which would logically explain as well why people with T2DM are more likely to develop or suffer from CHD. Insulin resistance causes elevated triglycerides and a reduction on HDL-c, as well as an increase on glycation of proteins, an increase in arterial blood pressure, increase inflammation and hypertension, all factors linked to increased risk of atherosclerosis (5).

Since the LDL-c hypothesis as a vera causa has been disproven, and until the IR hypothesis is disproven, if that time ever comes, reversing IR seems like the best course of action, and the implementation of LCHF has been shown promising results in doing so. In recent studies, LCHF diets have been demonstrated to be a highly effective way to reverse metabolic syndrome, to reduce triglycerides levels, to promote weight loss and to help reduce or even stop diabetes medication (2). 

Bibliography

1.         Taubes G. Rethinking Diabetes. London: Granta Publications; 2024. 495 p.

2.         Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ, Westman EC, et al. Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base. Nutrition. 2015 Jan;31(1):1–13.

3.         Subbotin VM. Excessive intimal hyperplasia in human coronary arteries before intimal lipid depositions is the initiation of coronary atherosclerosis and constitutes a therapeutic target. Drug Discov Today. 2016 Oct;21(10):1578–95.

4.         Subbotin VM. Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis. Theor Biol Med Model. 2012 Dec;9(1):11.

5.         Noakes T, editor. Ketogenic: the science of therapeutic carbohydrate restriction in human health. London San Diego, CA: Academic Press, an imprint of Elsevier; 2023. 1 p.

6.         Harcombe Z, Baker JS, Cooper SM, Davies B, Sculthorpe N, DiNicolantonio JJ, et al. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart. 2015 Jan;2(1):e000196.

7.         Ravnskov U, De Lorgeril M, Diamond DM, Hama R, Hamazaki T, Hammarskjöld B, et al. LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature. Expert Rev Clin Pharmacol. 2018 Oct 3;11(10):959–70.

8.         Barter P, Gotto AM, LaRosa JC, Maroni J, Szarek M, Grundy SM, et al. HDL Cholesterol, Very Low Levels of LDL Cholesterol, and Cardiovascular Events. N Engl J Med. 2007 Sep 27;357(13):1301–10.

9.         Austin MA, Hokanson JE, Edwards KL. Hypertriglyceridemia as a Cardiovascular Risk Factor. Am J Cardiol. 1998 Feb;81(4):7B-12B.

10.       Norwitz NG, Soto-Mota A, Kaplan B, Ludwig DS, Budoff M, Kontush A, et al. The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted Diets. Metabolites. 2022 May 20;12(5):460.