Sugar, Refined Grain and Seed Oil: The Mechanism Behind Each One

There is no such thing as an essential carbohydrate. There is no biochemical reaction in the human body that requires dietary fructose — not one.

Every other macronutrient class has essential forms. There are essential amino acids and essential fatty acids; deprive someone of those and they develop a deficiency disease. Added sugar has no essential form. You could eliminate it entirely and develop no deficiency of any kind.

This article takes the three dietary drivers one at a time and gives the mechanism for each — including, at the end, an honest account of where this evidence is weaker than it is usually presented.

Blood glucose is the smoke, not the fire

Pre-diabetes and type 2 diabetes are diseases of insulin resistance. The sequence runs: excessive insulin production first, elevated blood glucose later, once the compensation begins to fail.

Which means blood glucose is a late marker. Treating the glucose number without addressing the insulin resistance underneath is treating the smoke.

Now hold that beside standard dietary guidance for people with diabetes, which has historically recommended something close to 55% of daily calories from carbohydrate, much of it starch. We advise people with a carbohydrate-processing disorder to build their plate around carbohydrate, then escalate their medication when glucose rises exactly as the physiology predicts.

Refined carbohydrate raises blood glucose, raises medication requirements, and promotes weight gain. None of those three effects is controversial.

Carbohydrate restriction, and how strong that evidence is

A 2015 position paper by Feinman and twenty-five co-authors argued that dietary carbohydrate restriction is the single most effective intervention for reducing the features of metabolic syndrome, and should be the first approach in managing type 2 diabetes.¹

Below roughly 10% of calories from carbohydrate — a ketogenic range — the largest reductions in HbA1c and in medication requirement are seen, and critically these occur independently of weight loss. The metabolic improvement is not simply a consequence of becoming smaller; it follows from removing the input.

An honest qualification: this is a position paper — a considered argument assembled by a group of researchers, not a single randomized trial. It should be weighed as such. The trial evidence behind it has continued to strengthen, but a position paper and an RCT are different things and deserve different confidence.

A safety point that matters here. Carbohydrate restriction lowers blood glucose quickly. If you take insulin or a sulfonylurea, doing this without supervision risks hypoglycemia, and SGLT2 inhibitors carry a specific risk of euglycemic ketoacidosis. Medication doses often need adjusting downward as the diet changes. Do not start, stop, or change any medication without consulting your physician.

Sugar, independent of calories

Robert Lustig’s position is that sugar contributes to type 2 diabetes independently of its calories and independently of its effect on body weight.²

That is a strong claim, so look at the experiment behind it. Lustig’s group took children with obesity and metabolic syndrome and restricted fructose while holding total calories constant. Same calories in. Weight held stable. The only variable changed was fructose. Within nine days, markers of metabolic health improved significantly.³

That is about as clean a demonstration as nutrition research produces. When calories are fixed and one molecule is changed, whatever improves is attributable to that molecule.

On the population side, added sugar intake is associated with increased cardiovascular disease mortality among US adults, in a dose-response relationship.⁴

Oxidized linoleic acid, and where the evidence stops

Industrial seed oils have been a meaningful part of the human diet only since about 1917. Against two to three million years of hominin eating, that is essentially nothing.

The specific concern is linoleic acid, the dominant omega-6 fat in these oils. Linoleic acid is chemically fragile and oxidizes readily. That is why oils go rancid, and oxidation does not stop at the point of swallowing.

Context matters enormously. In whole foods — seeds, nuts, fish, eggs — linoleic acid arrives alongside vitamin E and other antioxidants that protect it. Extract it, heat it, deodorize it and bottle it, and the protection is stripped away while the fragile molecule is concentrated.

Ramsden and colleagues recovered lost data from the Sydney Diet Heart Study, in which 458 men replaced saturated fat with safflower oil. Mortality in the intervention group was higher than in controls. When those recovered data were incorporated into an updated meta-analysis of linoleic acid intervention trials, the risk of coronary heart disease death trended upward — hazard ratio 1.33, 95% confidence interval 0.99 to 1.79, P = 0.06.⁵

That P value does not clear the conventional threshold for statistical significance. The confidence interval crosses 1.0. This evidence points; it does not prove. The authors’ own conclusion was that the findings “could have important implications” for advice to substitute omega-6 for saturated fat — which is exactly the right strength of claim, and stronger claims than that are not supported.

What I will not claim about cancer

Older data suggesting omega-6 oils were protective was confounded, because it grouped omega-3 intake together with omega-6, and omega-3 was doing the work.

There is also an older literature on cancer. The Los Angeles Veterans trial reported cancer mortality rising with omega-6 vegetable oil consumption, and animal work shows omega-6 promoting experimentally induced tumors while omega-3 inhibits them.

Here I stop short of where this material is usually taken. You will hear “cancer is a metabolic disease” stated as settled. It is not. It is a serious minority hypothesis under active investigation, and the older cancer signals from these trials have not replicated cleanly.

What is defensible is narrower and still worth acting on: metabolic dysfunction and oxidized omega-6 products are plausible contributors to cancer risk, they are being actively studied, and that is one more reason to remove these oils from your kitchen. A smaller true statement is worth more than a large one that cannot be defended.

Frequently asked questions

Key takeaways

• There is no essential dietary sugar and no biochemical requirement for fructose.
• Blood glucose is a late marker; insulin resistance is the earlier and more treatable problem.
• Carbohydrate restriction produces the largest HbA1c and medication reductions, independently of weight loss — from a position paper, not a single trial.
• Isocaloric fructose restriction improved metabolic markers in nine days with calories and weight fixed.
• The seed oil evidence trends toward harm but did not reach statistical significance (HR 1.33, P = 0.06).

Medically reviewed by Gurpreet Singh Padda, MD — Board Certified in Anesthesiology, Pain Medicine, Interventional Pain Management, Addiction Medicine, and Obesity Medicine. Last reviewed July 2026.

This article is educational and is not a substitute for evaluation, diagnosis, or treatment by a physician. Individual results vary. Do not start, stop, or change any medication without consulting your physician. To be evaluated, request an appointment or call (314) 481-5000.

References

1. Feinman RD, Pogozelski WK, Astrup A, et al. Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base. Nutrition. 2015;31(1):1–13.
2. Lustig RH. Sickeningly sweet: does sugar cause type 2 diabetes? Yes. Canadian Journal of Diabetes. 2016;40(4):282–286.
3. Lustig RH, Mulligan K, Noworolski SM, et al. Isocaloric fructose restriction and metabolic improvement in children with obesity and metabolic syndrome. Obesity. 2016;24(2):453–460.
4. Yang Q, Zhang Z, Gregg EW, et al. Added sugar intake and cardiovascular diseases mortality among US adults. JAMA Internal Medicine. 2014;174(4):516–524.
5. Ramsden CE, Zamora D, Leelarthaepin B, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ. 2013;346:e8707.

Dr. Gurpreet Singh Padda, MD, MBA, MHP