Brain Food: Treating and Preventing Alzheimer’s with a Ketogenic Diet

Ketogenic foods shaped into a brain

Health is like rolling a dice, it’s all chance. Or so we think. When it comes to Alzheimer’s disease, the odds are worrisome. One in every ten adults ages 65 and older suffer from the incurable condition, according to the Alzheimer’s Association. Many people accept these odds and fall into the misconception that developing Alzheimer’s is out of their control. But all of us, including those that are genetically predisposed to the condition, can control what we eat. While our current diet seems to accelerate Alzheimer’s, the ketogenic diet (keto) has the potential to reverse its effects, so we might not have to leave it all up to fate.

Our brains are composed of millions of neurons, cells that communicate through electrical signals, that allow us to execute daily activities. Alzheimer’s interferes with this process by progressively damaging and destroying neurons, reducing cognitive functions and causing symptoms like dementia. As reported by the Alzheimer’s Association, this condition affects 5.8 million Americans and the figure is projected to rise to 14 million in the next 30 years, as our population ages.

Image of a healthy eating plate, divided into vegetables, whole grains, fruits, and healthy protein.

The healthy eating plate shows a typical distribution of nutrients in a balanced diet.

If you observe a healthy eating plate, you will see that most of our caloric intake derives from carbohydrates (55%), followed by fats (30%) and proteins (15%). Our bodies convert the glucose sugars that constitute these carbohydrates into acetyl coenzyme A (Acetyl-CoA), a process called glycolysis. Next, we turn this molecule into adenosine triphosphate (ATP), a form of stored energy that is readily available for future consumption. Along with energy, this “balanced” western diet also provides us with essential vitamins and has many health benefits. While this nutritional plan seems favorable for living a healthy life, it contributes some of the most evident signs of Alzheimer’s.

Although the exact cause of Alzheimer’s is unidentified, scientists do know that the inability to metabolize glucose is one of the first manifestations of the disease. This impairment, which can occur as early as young adulthood, is triggered by the high carbohydrate consumption of our modern diets. Excessive blood glucose levels damage the ApoE lipoproteins (ApoE) that transport food to astrocytes, the cells of the central nervous system that in turn nourish neurons. As a result, neurons suffer from energy scarcity and die. Therefore, continuing to consume a high-carb low-fat diet with an impaired glucose metabolism, only enhances this process.

Increased levels of amyloid (Aβ) plaques, protein fragments released by the brain as metabolic waste, also contribute to neuronal cell death and Alzheimer’s by interfering with neural synapses. High-carb low-fat diets are an indirect cause of this large accumulation because of ApoE’s secondary function: regulating the dissolution of Aβ plaques. Because they are damaged by high blood glucose concentrations, ApoE are less capable of eliminating plaques when the brain produces high levels of waste, stunting interneuron communication and creating a toxic environment. In other words, our current diets are detrimental because they impair ApoE, which feed neurons and remove excessive Aβ plaques.

Clearly, carbs are the ones to blame and swapping this main source of energy is a plausible solution. Believe it or not, the ketogenic diet, currently one of the most popular weight loss trends, has shown to alleviate the effects of impaired glucose metabolism and decrease the number of Aβ plaques in our bodies. This diet, first designed to treat refractory child epilepsy, is constituted by a large percentage of fats (85%) and lower amounts of carbohydrates (8%) and proteins (7%). The absence of carbohydrates forces the body to turn to lipids for energy.

Under a state of “ketosis” the body bypasses glycolysis and undergoes β-oxidation. β-oxidation forms ketone bodies from lipids. These are then converted into Acetyl-CoA, the same end product glycolysis forms from glucose. From there on, the body continues its normal metabolic processes to create ATP, molecules of stored energy. Thus, supplementing glucose with ketone bodies leads to a positive cascade effect: the blood glucose concentrations decrease, ApoE are preserved, neurons are well-nourished and Aβ plaque production is regulated.

Studies carried out on animal models further support the positive medical benefits of keto. In Van der Auwera’s study, levels of Aβ plaques in mice brains decreased by 25% after 48 days of being on the keto diet. Similarly, Kashiwaya’s long-term administration of ketones to mice, inducing ketosis, not only resulted in plaque decline but also improved their cognitive functions.

Two other factors that contribute to Alzheimer’s are chronic neuroinflammation and oxidative stress. Neuroinflammation is the brain’s immune response to physical injury, neurotoxic substances, and even high concentrations of protein fragments (such as Aβ plaques). When this immune response is prolonged, it interferes with neuronal communication and leads to cell death. Oxidative stress is a bit more complicated.

As our brain consumes oxygen to undergo metabolic processes, it generates free radicals. These highly reactive molecules carry out important cognitive functions, but in excess, they can damage and even kill cells. As a form of protection, our bodies produce antioxidants to control the number of radicals. However, if this counteractive process is disrupted by physiological and environmental factors, we experience oxidative stress, an imbalance between the production and withdrawal of free radicals. As previously mentioned, the disproportionate number of free radicals leads to cell death.

Not surprisingly, the ketogenic diet’s anti-inflammatory and antioxidant properties make it a wonderful counteractor. Ketones, especially β-Hydroxybutyrate, can lower neuroinflammation by inhibiting the multiprotein complexes, or inflammasomes, that activate inflammatory responses. Ketones also reduce oxidative stress by activating Nrf2, a protein that senses and regulates antioxidant defense. In sum, ketones help prevent neuronal death by restricting our body’s inflammatory responses and controlling the amount of free radicals.

Now, let’s discuss what we all fear, yet is out of our control: genetics. If Alzheimer’s disease runs in your family, you might be thinking there’s no use in adopting a ketogenic diet. But don’t give up so easily. While inheritance does increase one’s risk of developing Alzheimer’s, it does not assure its development. Therefore, the same rules apply to those that carry the genetic marker, the ApoE4 allele. Recent evidence even suggests that keto can successfully treat patients that are genetically predisposed to Alzheimer’s.

In a case study conducted by Morrill and Gibas, a 71-year old female with the ApoE4 allele and a mild diagnosis of Alzheimer’s improved her cognitive test scores after undergoing a 10-week high-fat low-carb nutrition plan, supplemented with exercise and brain training. This dietary intervention, which increased the woman’s level of ketone bodies, supports the idea that nutrition can have a profound impact on the cognition of patients with genetic links to Alzheimer’s.

Undoubtedly, the ketogenic diet can provide us with advantageous consequences that help treat and prevent Alzheimer’s disease. But we must be aware of its drawbacks. Adverse effects, such as nausea, reduced appetite, decreased bone density, weight loss, and mineral and vitamin deficits, have been observed in some patients. Additionally, little is known about the health complications that may arise from a long-term use as well as the effects the ketogenic diet can have on patients with coexisting diseases. Furthermore, many argue that the changes in eating habits are difficult to sustain and tolerate over long periods of time.

More research must be conducted to determine the risks of the ketogenic diet and conclusively establish it as a method of treatment and prevention. However, adhering to this strict diet is simply a matter of desire. It is often believed that the ketogenic diet is monotonous. But with simple swaps, it is evident that there are many food options for those on keto. To help people in their food choices, apps like Nutrita provide keto-friendly suggestions and even full-course meals. There are many tools available to those wanting to transition into this type of diet.

For now, adopting a ketogenic lifestyle is promising. Not only does it seem to improve the cognitive functioning of patients with Alzheimer’s, slowing the disease’s progression, it also has the potential to lower the risk of development for those lucky enough to possess a clear mind. If you believe in these effects, you might want to give it a chance or stay tuned for future findings.

By: M. Torras


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Image Credits:

Image 1: Malan, David. “Food resembling a brain.” Getty Images,

Image 2: “The Healthy Eating Plate.” Harvard T.H. Chan School of Public Health,

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