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Is cooked meat linked to increased dementia risk?

Cooking meat “may” increase the risk of developing dementia, reports BBC News.

The claim  follows a study by US researchers on mice and humans, looking at what are known as advanced glycation end products (AGEs) and whether they are linked to the development of dementia and metabolic syndrome (a group of risk factors associated with the development of cardiovascular disease).

AGEs have been described as “rogue molecules”. These are compounds that can cause damage at the cellular level, specifically through a process called oxidation, which is best described as a form of biological rust.

AGEs are naturally produced in the body, but are also found in food. AGEs are present in foods, such as meat and eggs, and certain methods of cooking, such as grilling, broiling, roasting, searing and frying – the result is the formation of new AGEs.

The researchers compared mice fed a high AGE diet and mice fed a low AGE diet. Older mice fed a high AGE diet experienced changes in their brains, including a build-up of amyloid protein – a characteristic of Alzheimer’s disease in humans.

The mice in the high AGE diet group went on to develop symptoms similar to Alzheimer’s, such as problems with their balance and coordination.

Older mice fed a high AGE diet also experienced metabolic changes, characteristic of metabolic syndrome in humans.

The researchers then looked at 93 people aged 60 or older. High levels of AGE in the blood were associated with cognitive decline and reduced insulin sensitivity nine months later. However, none of these people actually developed diagnosed dementia or metabolic syndrome.

Overall, the results suggest there could be a link between AGEs and dementia and metabolic syndrome, although experts have said there are no “definitive answers”. 

Ideally, larger cohort studies should now be carried out into a possible link.

Where did the story come from?

The study was funded by the US National Institute of Health and carried out by researchers from The Icahn School of Medicine at Mount Sinai (US); the University of Connecticut (US); the University of Pavia (Italy); and the George Institute (Australia).

The study was published in the peer-reviewed journal PNAS.

What kind of research was this?

The research could be split into two parts.

The first was a laboratory study in mice, which aimed to see whether advanced glycation end products (AGEs) eaten in the diet predispose mice to dementia and metabolic syndrome and whether cutting out AGEs from a diet can prevent these conditions. The researchers did this by comparing mice fed a diet low in AGEs with mice fed a diet high in AGEs.

The researchers then looked to see whether a similar situation occurred in humans, by performing a small cohort study. The aim of this was to see if AGE intake in the diet and AGE levels in the blood were associated with changes in cognition and insulin sensitivity (the latter often being a precursor to type 2 diabetes and metabolic syndrome in humans).

Although the researchers used ideal methods for this early stage research, further research in humans is required to confirm the link.

What did the research involve?

Mice were fed one of three diets:

  • a diet low in AGEs (MG-)
  • a diet supplemented with a specific AGE (the AGE chosen was methyl-glyoxal derivatives [MG]) (MG+)
  • a normal diet

Each of the diets contained the same number of calories. This allowed researchers to explore the link between AGEs eaten in the diet and dementia without manipulating calorie intake, with the research conducted on mice with similar genetic backgrounds.

The researchers examined mice when they were 18 months old. They looked at levels of proteins in the brain, testing motor coordination, balance and motor learning, as well as object recognition and placement memory.

The researchers then looked at the association between dietary AGE intake/levels of AGEs in the blood and changes in cognition and insulin sensitivity over nine months in 93 people aged 60 or older.

What were the basic results?

Older (18-month-old) mice fed the MG+ diet had metabolic changes (including changes in their blood glucose and insulin levels and their body weight).

They also experienced changes in the brain, including:

  • deposits of AGEs in the brain
  • reduced levels of an enzyme called SIRT1 and changes in the levels of other proteins in the brain – this suggests that the AGEs were causing cellular changes to the brain
  • increased levels of amyloid-42 in the brain (the protein that builds up in plaques in Alzheimer’s disease)
  • gliosis (a process when glial cells, the support cells for brain cells, are activated and multiple, in response to damage)

These changes were not due to ageing or caloric intake, as neither these changes nor the metabolic syndrome occurred in mice fed the MG- diet.

Older mice fed the MG+ diet also had impaired motor coordination and balance learning compared to mice fed the MG- diet. Mice fed the MG+ diet also had poorer object recognition than mice fed the MG- diet.

In people, high levels of MG in the blood (which were associated with higher dietary intake of AGEs) predicted  cognitive decline nine months later, based on the results of the Mini Mental State Examination (a screening tool for early-stage dementia). This association remained after adjusting for age, sex, education and baseline score on the Mini Mental State Examination.

Levels of MG in the blood also correlated with reduced insulin sensitivity, which is often an early “red flag” warning that a person is at risk of developing metabolic syndrome.

How did the researchers interpret the results?

The researchers conclude that age-related dementia and metabolic syndrome may be causally linked to high levels of food AGEs, specifically MG.

They also state that because AGEs can be modified in humans, recognition of this risk factor may open unique therapeutic avenues.

Conclusion

In this study, researchers compared mice fed a high AGE diet and mice fed a low AGE diet, suggesting that high AGEs may be linked to the development of dementia and metabolic syndrome.

Older mice fed a high AGE diet experienced changes in their brains (including a build-up of amyloid protein, which is a characteristic of Alzheimer’s), and had problems with coordination, balance, learning and poorer object recognition compared to mice fed a low AGE diet. Older mice fed a high AGE diet were also found to have metabolic changes (including changes in their blood glucose and insulin levels, as well as their body weight).

However, despite these changes to the brain and metabolism, it cannot be said that the mice actually developed the human equivalent of either dementia (Alzheimer’s or other), or metabolic syndrome.

Similarly, there was not a single diagnosis of Alzheimer’s or metabolic syndrome in the human part of the study.

In this section, they looked at 93 people aged 60 or older. They found that high levels of AGE in the blood (which were associated with a higher dietary AGE intake) predicted cognitive decline over nine months and reduced insulin sensitivity. However, this analysis was greatly limited by the small sample size and the fact none of these people actually developed diagnosed dementia or metabolic syndrome.

The results suggests a potential link between dietary intake of AGEs and dementia and metabolic syndrome.

However, further research is required to confirm the link in humans.

However, eating a diet rich in fish, legumes, low-fat milk products, vegetables, fruits and whole grains will help protect your heart, if not your brain. Read more about healthy eating.

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