BALLARD OF SUGAR (PART 2)

BY: DR. BAYNE FRENCH MD DC
(Continuation, referencing Ballard of Sugar Part 1)

TEN. Advanced Glycation Endproducts (AGEs)

The article describes Advanced Glycation Endproducts (AGEs) as an emerging topic in the development of metabolic diseases associated with modern diets (Aragno et al., Nutrients, 2017).

AGEs are described as toxic compounds that form when sugar reacts with body tissues. The article cites Uribarri et al. (Journal of the American Dietetic Association, 2013), stating that AGEs can promote oxidative stress and inflammation by binding to cell-surface receptors or by cross-linking proteins, which can alter protein structure and function.

The article explains glycation as the process where sugar binds to proteins, fats, and DNA. It uses HbA1c (haemoglobin A1c) as an example, describing it as a measure of glycation in red blood cells and noting its use in diabetes management. The author presents HbA1c as an indicator of metabolic health and disease risk.

The article states that glycation occurs in everyone and increases with age, and that higher blood sugar levels increase the rate of glycation. It presents regular sugar intake as a key factor in accelerating this process.

The article restates that sucrose is made of glucose and fructose and says both can drive glycation and AGE formation, but that fructose is more potent. It cites Bunn et al. (Science, 1981), stating fructose caused 7.5 times more glycation than glucose. It also states that a fructose breakdown product, methylglyoxal, drives glycation 250 times faster than glucose.

The article adds that sugar both increases AGE formation and reduces the body’s ability to detoxify AGEs by interfering with enzyme function. It quotes Dr Robert Lustig, from the book Metabolical: “All in all, when it comes to aging, fructose is worse than glucose, and therefore sugar is worse than starch”.

ELEVEN. Dr Volek

The article references Dr Volek and the FASTER study (published in Metabolism, 2016). It describes the study as comparing athletes adapted to high-carbohydrate fuelling with athletes adapted to lower-carbohydrate fuelling, measuring multiple outcomes.

It reports the following results as presented in the article:

• The lower-carbohydrate group had nearly 2% lower body fat and over 3 kg more lean mass.
• VO₂ max was similar between groups.
• The lower-carbohydrate group had 2.3-fold higher fat-burning rates than the high-carbohydrate group.

TWELVE. Insulin

The article describes insulin as a major regulator of metabolism and states that insulin receptors are present on the surface of the body’s cells. It states insulin is necessary for life and has beneficial effects, but that chronic elevation is linked to metabolic problems and disease.

The article lists two major negative effects it attributes to chronically elevated insulin:

• Reduced fat burning and increased fat formation.
• Increased cell proliferation, increasing risk of cardiovascular disease (Fu et al., Molecular Metabolism, 2021; Patil et al., Missouri Medicine, 2012) and cancer (Leitner et al., Biochemical Journal, 2022).

It states that elevated blood sugar is the most potent driver of increased insulin.

THIRTEEN. Dementia

The article defines dementia as progressive loss of cognitive ability and states incidence is increasing, with Alzheimer’s disease as the most common form.

It references another article by the author (“Sugar and its Role in Dementia. Avoid Getting Stupiderer”) and states that regular sugar intake contributes to reduced cognitive function. It then notes that sugar is associated with cardiovascular disease, inflammation, type 2 diabetes, and obesity, and argues that dementia risk increases with those conditions, meaning sugar may indirectly increase dementia risk.

It also lists studies described as showing cognitive impacts of sugar independent of other diseases:

• Highest sugar consumers had smaller brains and worse memory (Pase et al., Alzheimer’s & Dementia, 2017).
• Highest female sugar consumers had the highest Alzheimer’s risk (Liu et al., Nutritional Neuroscience, 2022).
• Highest sugar consumers had the lowest Mini Mental Status Exam scores (Chong et al., Clinical Interventions in Aging, 2019).
• Sugary drink consumption damages cognitive ability (Liu et al., Journal of Affective Disorders, 2022; Sun et al., Journal of Prevention of Alzheimer’s Disease, 2022).
• For each 10% increase in calories from sugar, dementia risk increased by 40% (Agarwal et al., Journal of Alzheimer’s Disease, 2003). The article states the highest sugar consumers developed dementia 7.1 years earlier and consumed an average of 106 g/day. It contrasts this with endurance fuelling advice recommending at least 90 g of sugar per hour.
• Zhang et al. (BMC Medicine, 2024) studied over 200,000 people and reported that sucrose was most strongly associated with all-cause dementia and Alzheimer’s disease, with the highest sugar consumers having the highest dementia incidence.

FOURTEEN. Fatty Liver Disease (FLD)

The article describes fatty liver disease as commonly identified on ultrasound reports and also refers to it as NAFLD (non-alcoholic fatty liver disease). It states it is widespread and increasing, and that it is associated with inflammation, scarring, cirrhosis, and liver cancer. It states sugar is a major driver through several mechanisms:

1.   Increased lipogenesis (fat formation): fructose (half of sucrose) and uric acid (formed from fructose) stimulate lipogenesis, increasing fat storage in the liver.

2.   Impaired beta-oxidation (fat burning): the processes that increase fat formation also reduce fat burning, which the article links to obesity and poorer athletic performance.

3.   Uric acid: fructose is described as the only sugar that increases uric acid, and uric acid is described as directly contributing to fatty liver disease. The article states sugar contributes directly via fructose and indirectly via uric acid.

4.   Intestinal lining damage: the article states fructose damages tight junctions, increasing gut permeability and allowing bacterial toxins to reach the liver, increasing immune activation and long-term scarring.

5.   “Gut training”: described as increasing sugar intake to increase transporters for glucose and fructose, increasing absorption, with the liver receiving the initial load.

The article rejects the claim that exercise prevents sugar-related harm and states there is no evidence supporting that claim.

It then references Nirengi et al. (2018, Frontiers in Endocrinology), describing a comparison between 69 elite rugby players (training 18 hours/week) and 29 non-rugby participants. It states:

• 1 in 5 rugby players had evidence of fatty liver disease.
• None of the non-athletes had fatty liver disease.
• Rugby players had higher triglycerides, worse cholesterol profiles, and higher total fat mass.
• Rugby players consumed 500–750 g of carbohydrate per day, while the non-athletes consumed less.

It characterises “sugar is only harmful if you don’t exercise” as incorrect.

FIFTEEN. Increased gut permeability

The article states the intestinal barrier is very thin and separates gut contents from the bloodstream. It argues that increased permeability (“leaky gut”) increases the risk of multiple diseases.

It cites Lambertz et al. (Frontiers in Immunology, 2017), describing “fructose induced alterations of the tight junction proteins”, increasing permeability and allowing bacteria and endotoxins to enter the bloodstream.

It also mentions adherens junctions and desmosomes as proteins involved in maintaining the barrier, and states sugar is toxic to these proteins. The article also states fructose alters gut flora towards pro-inflammatory microbiota that release toxins such as lipopolysaccharide (LPS), further damaging the intestinal barrier.

It states the liver is the first major target organ, and that distant organs such as the brain may also be affected.

Conclusion (as presented)

The article quotes Sun Tzu: “know thy enemy”. It argues that people seeking a longer health-span and life-span, or athletes seeking peak performance, a longer career, and fewer injuries, should understand factors that drive inflammation and reduce metabolic health.

It states that the article listed 15 examples of how regular sugar intake damages biochemistry and metabolism. It states individuals are responsible for their health and should challenge advice that promotes “more is better”.

It repeats the phrase: Optimal human performance is a direct result of optimal metabolic wellness. It restates that the article considers sugar “toxic” and characterises advice to consume high amounts of sugar as unacceptable.

The author closes with a personal reflection on ageing and the need to act on nutrition knowledge, and states that reducing regular sugar intake is an important starting point.