Carnivore for Alzheimer’s Prevention – A No Brainer

Globally, every three minutes, someone develops dementia. By 2050, an estimated 152 million people will have dementia. So chances are you know someone – a parent, grandparent, or friend – has as suffered from this horrible disease as well. But contrary to popular belief, Alzheimer’s Disease (AD) is not a normal part of aging. It can be prevented. The key is to take action as soon as possible since it’s thought that AD begins 20 years or more before symptoms arise. Keep reading to learn more about the causes of dementia and the choices you can make to avoid this terrible disease.

What is Alzheimer’s Disease?

AD is a progressive neurodegenerative disease characterized by the progressive decline of memory, cognitive functions, and changes in behavior and personality. Sadly, AD is the 6th leading cause of death in the United States and the 5th leading cause of death for those aged 65 and older. AD is the most common type of dementia, a category of mental impairment that also includes cerebrovascular disease (vascular dementia) and Lewy body dementia.

What are the Risk Factors for Dementia?

Dementia can be prevented and, in some cases, early symptoms can be reversed. Risk factors for dementia can be categorized into modifiable and non-modifiable. Non-modifiable risk factors include age, genetics, gender (women are more likely to have Alzheimer’s), and a positive family history of dementia since more than one-third of AD patients have one or more affected first-degree relatives.

The good news is that there are modifiable risk factors – areas where our choices can mitigate dementia. Modifiable risk factors include avoiding smoking, head injury, environmental factors, and metabolic syndrome (MetSys), one of the fundamental causes of dementia. MetSys is a signal that the body is not properly handling carbohydrates and is, therefore, a risk factor for obesity, Type 2 diabetes, heart disease, and hypertension. Treating MetSys minimizes the risk of Alzheimer’s and other dementias in 40% of the population.

Alzheimer’s Dementia is a Metabolic Issue

While the cause of AD is multifactorial, with both genetic and environmental factors implicated in its pathogenesis, AD is arguably a metabolic issue that stems from the brain’s inability to harness energy from glucose. In addition to these lifestyle choices, we can modify (lower) our risk of AD through dietary choices.

The brain is an energy-hungry organ. Although it only typically accounts for 2% of body weight, it can require up to 20% of the body’s glucose and oxygen. That’s why adequate fuel delivery is so important. Compared to healthy people, those with AD have been found with up to a 45% reduction in the cerebral metabolic rate of glucose or CMRglu. This results in reduced fuel usage by brain regions responsible for memory processing and learning. Because areas of the brain dedicated to visual and sensorimotor processing are unaffected, it can be difficult to notice changes, even though the risk of developing AD is present. A decline in glucose metabolism can be detected decades before overt symptoms.

Type 2 v Type 3 Diabetes

You may have heard the terms “Type 3 diabetes” or “diabetes of the brain” because similar to Type 2 diabetes, the brain becomes incapable of adequately metabolizing glucose due to insulin resistance (or insulin insensitivity). Without adequate fuel, neurons in regions of the brain start to degenerate. Degraded neurons eventually become incapable of communicating, leading to symptoms associated with AD such as confusion, cognitive decline, and behavioral changes.

Type 2 and Type 3 diabetes are related in that they may have the same primary underlying cause of insulin resistance, but they are not the same. An individual does not need to be diagnosed with Type 2 diabetes in order to develop Type 3 or AD. In fact, many people with AD have normal blood glucose levels and are not diagnosed with diabetes. The key factor is, therefore, not glucose, but insulin resistance, a reduction in the body’s sensitivity to insulin, and hyperinsulinemia (elevated levels of insulin in the bloodstream for extended periods of time.) These disturbances lead to inflammation and oxidative stress, an imbalance of free radicals which can create damage to the cells and tissue in the body. While Type 2 diabetes affects muscles, organs, and the rest of the body aside from the brain and central nervous system, damage from AD is localized to the brain.

Insulin and Beta-amyloid Plaques

Interestingly, insulin also plays a crucial role in the formation of amyloid plaques, protein fragments that accumulate in the brain. While these plaques are found in healthy brains, in AD patients, beta-amyloid plaques accumulate to an unhealthy level, interfering with cell communication. Aside from reduced glucose utilization, beta-amyloid plaques are one of the defining features of AD.

One theory as to why these plaques accumulate in the AD brain is that they are not broken down and cleared away as they should be. Beta-amyloid plaques are primarily cleared with insulin-degrading enzyme, the same enzyme the body uses to clear insulin once insulin has done its job. Because the enzyme prefers insulin to beta-amyloid plaques, it works on clearing insulin first, leaving plaques to accumulate. Chronically-elevated insulin levels lead to more plaque build-up. And the more it builds up without being cleared, the more likely it is to form plaques that interfere with neuronal communication.

The Importance of Early Alzheimer’s Disease Prevention

This article cannot overstate the importance of AD prevention. AD begins with small changes in the brain that are initially unnoticeable to the person affected. Only after years of brain changes do individuals experience noticeable symptoms, at which point disease reversal may be too late. While there is no cure for AD, it can be prevented through dietary and lifestyle interventions. Consider prevention a lifelong concern. Waiting for an AD diagnosis may be too late – the brain may have already suffered too much damage.

Dietary Changes for AD Prevention

Carbohydrate restriction by way of a carnivore, keto, or ketosis-inducing diet is one of the first steps we can take to begin to ease the metabolic dysfunction that causes AD. If the brain has become incapable of properly metabolizing glucose, then a low or no-carbohydrate diet utilizing another fuel source can help correct abnormalities. This alternate fuel source – ketones – are generated when the body switches from metabolizing carbohydrates to metabolizing fat. In a low insulin environment, the body will produce ketones, a product of fat burning, to provide the brain with nourishment.

“The therapeutic and neuroprotective effects of ketones are so impressive, in fact, that one of the premier researchers studying ketones and brain health has suggested that a drawback of the modern, carbohydrate-heavy diet is that is it ‘keto-deficient.’” 

The Alzheimer’s Antidote

While the causes of AD are multifactorial, dietary changes can play a significant role in preventing or even reversing AD symptoms. The price of poor brain health is too high to delay starting to pay attention today. To learn more about Alzheimer’s prevention using a low-carb diet, please refer to Amy Berger’s book, The Alzheimer’s Antidote.

Written by Laura Guy
I dedicate this article to my father, Stuart. I love my father dearly and have watched him transition from an ambitious, independent man to an immobile and totally dependent man with very little speech capacity. Sadly, he has experienced very little quality of life over the past 11 years due to the degenerative effects of dementia, a disease for which there is no cure.