Our Keto Journey Part 2: Getting Rid Of Stubborn Pounds And Guarding Against Alzheimer’s

In the first post in this series, John presented a 5,000-foot view of what a ketogenic diet looks like. If you’re completely unfamiliar with a keto diet, we suggest you read that post first. In this post today, I’ll share why I went keto. In the next post, John will be sharing his story.

The important takeaway in these next two posts is that not everyone goes on a keto diet for the same reasons. Some go on it to treat a specific illness while some go on it because it may have the potential to prevent certain diseases. Others go on it because they want to lose a lot of weight quickly, some believe it’s a healthy way of eating, and others are seeking enhanced sports performance.

Let me tell you why I decided to go keto and why you may want to consider it too.

Why I Went Keto

John always jokes that when we first met, we’d go out to lunch and I’d always order the big salad. Seinfeld wasn’t a thing yet so I wasn’t copying Elaine.

I’ve been a low-carb eater since I was a teen. Obesity and type 2 diabetes run in my family, and that’s something I’ve fought hard to avoid my whole life.

Preventing weight gain was an ongoing battle for me, and I fought it by limiting carbs.

However, after I had four children, you can guess what happened. Yes, I put on the inevitable extra pounds. Since I was still going low-carb, I lost some of the weight, but there were still 20 stubborn pounds that refused to leave.

When I turned 60, still low-carb and after 3 years of strength training, those pounds had increased to 23. And I just couldn’t lose them. Now, 23 pounds may not seem like a lot to some. But when you’re 5’1” and those pounds show up in the wrong places, you want them gone with a passion. But even more so I wanted those pounds gone because I knew I would feel better and be a better version of myself overall.

So, I needed to take a more radical approach.

That’s why I turned to a keto diet.

Ultra Low-Carb Diets Result In Fat Loss

By now it’s no secret that low-carb diets promote fat loss. When you consume carbs, they’re turned into glucose in your digestive tract which is then sent into your bloodstream. Your pancreas releases insulin which takes the glucose out of your bloodstream and sends it to your cells to be used as energy.

However, if you’re eating excess carbs and your cells have enough glucose for energy, insulin acts as a storage hormone and packs that glucose into your cells where it’s converted to fat.

Now, if you continue to consume excess carbs, particularly refined carbs (like pasta, bread, rice, sugar, and fructose) and carb dense veggies like potatoes, over a long span of time (years), insulin will not only continue to pack glucose into your cells, it will lock it in and you’ll get fatter. This is called the Carbohydrate-Insulin Model of weight gain.

But, here’s a bigger problem. If you continue to eat excess refined carbs long enough whereby insulin is constantly spiked, then it can lead to serious conditions such as insulin resistance, obesity, and type 2 diabetes.

However, if you engage in carb restriction and decrease insulin secretion, then eventually you’ll lose fat. And the stricter your carb restriction, the more weight you should lose in a quicker amount of time.

So, in order to lose the excess weight quickly, I decided to go keto. As John mentioned last week, the ketogenic diet is ultra low-carb (<30 net carbs/day). At this amount of carbs, fat loss should happen quickly.

Before I go any further there’s something important I want to point out that has seemed to confuse many individuals who consider going keto.

If You Just Want To Lose Fat You Don’t Have To Go Keto 

Here’s the thing. If you just want to lose fat, you don’t have to go keto. You don’t have to produce ketones to lose a lot of weight quickly.

Since carbohydrate restriction and lowering the amount of insulin your pancreas is secreting are the important factors in weight loss, you don’t have to be concerned with ketone numbers. 

If you have a specific medical condition you’re trying to heal, sure go ahead and strive to produce ketone levels above 0.5mmol. But if you just want to lose weight, it’s not necessary.

That being said there was another reason why I wanted to be on a keto diet.

A Surprising Blood Test

Right before going keto, I had a blood panel done. To my surprise, my HbA1c (an average of 3 months blood glucose) was borderline pre-diabetic. That was a big surprise!

A high HbA1c probably indicated a certain degree of insulin resistance. How could that be after years of going low-carb? Answer: Maybe for my body, it wasn’t low carb enough.

So, in order to lose those extra pounds quickly and bring down my HbA1c, keto was the way to go. But my reasons didn’t stop there.

A Family History Of Alzheimer’s Disease

If you’ve had a family member or a close friend who has suffered from Alzheimer’s Disease (AD), you know how horrible the disease is.

My mom, Shirley, developed AD at 72 years old. For the next 10 years, I experienced all the pain and suffering of watching my once happy and vibrant mom have her memories, personality, and life drain away. It was devastating. My mom was my best friend.

Imagine having a conversation with your mom and out of the blue she says, “I don’t have any children.” You reply, “I’m your daughter. I’ll always be your child, and I need you to be my mom.” She responds with, “No, I don’t remember having you.” Whoa, stop, get out the kleenex. 

I don’t talk about this much because I get so choked up that I just can’t talk.

The sad thing is I wish I knew then what I know now. When my mom got AD, the doctors told us there was no treatment for the disease, and they had no clue why people got it. That meant that my mom would just get progressively worse.

Today, this is not the case. We now have good evidence showing that a keto diet can be a powerful tool for preventing and treating AD. I wish I’d known this when my mom was suffering from Alzheimer’s.

In order to get a good idea of why ketosis and a keto diet might be effective for AD, it’s important to have some knowledge of what the disease is all about. John wrote the following science section on Alzheimer’s. Since he’s a science geek, it may be a little science-heavy, but the information really helped me understand the disease.

Alzheimer’s Disease

Researchers are now beginning to discover that AD might actually be a metabolic disease mediated by the brain’s response to insulin. Growing evidence appears to confirm that AD is highly associated with poor glucose utilization and insulin resistance (IR) within the brain itself.

Many scientists are starting to refer to AD as brain diabetes or type 3 diabetes.

The important thing to understand is that AD is a problem of energy deficiency within the brain. The brain is simply not getting enough fuel to sustain its important functions. While our brains only constitute about 2% of our body’s mass, it uses about 20-25% of our total body’s energy. And it needs all that energy to function well.

If fuel is in short supply, brain neurons that work the hardest, those responsible for memory and cognition, will be among the first to suffer decline.

But here’s the big problem. Brain energy deprivation caused by poor glucose utilization and IR could begin in individuals as early as their 30s or 40s. This means that AD might start as a silent process that takes years to eventually manifest. By the time the disease is discovered, it could be too late to treat it successfully.

Below is a summary of the important risk factors for AD. Again, there’s some science here, but if you can get through it, you’ll really understand why ketosis can be an important therapy for Alzheimer’s patients. If you’re really not into science, scroll down to Your Brain And Ketones section.

Associated Risk Factors For AD

Advanced Age

As of 2017, there are approximately 5.3 million Americans over the age of 65 suffering from AD and approximately 200,000 individuals under age 65 have younger-onset AD. Thus AD appears to be a disease associated with old age. However, while symptoms usually manifest in advanced age the disease was probably active for decades.

The ApoE4 Gene

People who carry the ApoE4 gene are 4 to 15 times more likely to develop AD. However, not everyone who has the gene develops AD, and some people who have AD don’t even have the gene. Therefore, the gene is not sufficient to cause AD.

So, why is there an increased risk for AD in ApoE4 positive individuals? Doctors are not sure, but there is some evidence that a high carbohydrate Western Pattern Diet could induce the gene to cause pathology. See here and here.

Chronically Elevated Insulin Levels

A risk factor that seems to play an important role in AD is chronically elevated insulin levels, also known as hyperinsulinemia (see here, here and here).

Generally, when a person goes to their physician for a check-up, the doctor will perform a fasting blood glucose test (FBG). If your FBG is within normal limits, your doctor will conclude you don’t have diabetes.

If you have a really good doctor, they might perform a HbA1c blood test. This is a lot more reliable than a simple FBS. 

Now, this is where it gets tricky. As I mentioned before, a high Hb1Ac, but a normal FBG level is evidence of a degree of hyperinsulinemia and insulin resistance (IR). 

Unfortunately, doctors rarely check insulin levels. Therefore, an individual could have IR for years and never know it. This could mean that diseases closely linked to IR like type 2 diabetes, hypertension, gout, benign prostate hyperplasia (BPH), PCOS, and AD may be in their germinating phase.

We now suspect this was the case with Barbara’s mom. She was never diagnosed with diabetes, but her doctor told her to watch her sugar. Add this to the fact that she was overweight her entire life. She probably had insulin resistance for years before developing the symptoms of Alzheimer’s Disease.

There is now compelling evidence that AD is a form of brain diabetes. Like diabetes, AD exhibits altered glucose metabolism, inflammation, and insulin resistance.

Amyloid Beta (Aβ) Plaques

If you’re familiar with AD, you’ve probably heard that amyloid beta (Aβ) plaques play a major role in causing the disease. Aβ is a protein that is often secreted by neurons in response to an injury. Normally, this protein is removed by the glymphatic system.

Photo by: BruceBlaus

However, if Aβ is not removed, it can form plaques that block the synapses between neurons thus interfering with neuronal communication. Blocked signaling between neurons can lead to the symptoms found in AD such as cognitive decline and memory loss.

Here’s where things get interesting. While it’s true that individuals with AD have been found to have amyloid plaques, it’s also true that others who had AD didn’t have them. And some individuals who didn’t have AD were found to have Aβ plaques. See here.

While Aβ plaques could make AD worse, they’re probably not the main cause.

Concerning AD and Aβ plaques, the authors of this study concluded that,

Therefore, low regional CMRglc [glucose utilization] appears to be a very early event in the disease process, well before any clinical signs of dementia are evident, and well before cell loss or plaque deposition is predicted to have occurred.

See also here and here. So again energy deficit seems to be the be the big factor in AD.

Beta-Amyloid And Insulin-Degrading Enzyme

As I mentioned before, Aβ must be removed so as not to create plaques. Insulin-degrading enzyme (IDE) which degrades Aβ is important in this process. However, degrading Aβ is not IDE’s main purpose. Its main purpose is to clear excess insulin.

So, when an individual’s insulin levels are high, IDE’s main job becomes clearing insulin and its secondary concern, clearing Aβ is ignored. This could pave the way for increased Aβ plaques formation.

Interestingly, people with the ApoE 4 gene appear to produce less IDE.

Okay, what’s the takeaway here? Very simple. When it comes to Alzheimer’s risk, it’s mainly about insulin resistance, energy deficit in the brain, and many times the presence of the ApoE4 gene. Let’s see where the ketogenic diet comes in.

Your Brain And Ketones

As we’ve seen, Alzheimer’s Disease is primarily caused by poor glucose metabolism in brain neurons. Because neurons are prevented from using glucose as an energy source, they are essentially being starved to death.

Now, get ready for some good news. Glucose is not the only fuel your brain can use. It can also use ketones as an alternative energy source. Ketone metabolism by brain mitochondria isn’t impeded by the same factors that hamper glucose utilization.

While your brain will always metabolize some glucose, ketones can provide up to 60% of your brain’s energy. A blood concentration of 0.3–0.5 mMol of ketones, supplies 3–5% of whole brain energy requirements, a 1.5 mMol concentration provides about 18%, and at 6 mMol, they supply about 60% of brain fuel.

Theoretically, this means that ketones can supply a large part of brain energy which could theoretically limit cognitive decline.

But is there evidence that this is the case? There sure is.

A Ketogenic Diet Helps With AD

A small study of 23 older adults with mild cognitive impairment compared the effects of a high carbohydrate versus a very low carbohydrate diet (<35 grams) over the course of 6 weeks. The low-carb diet was designed to specifically cause ketosis.

Remember that an effect of an ultra low-carb high-fat diet is the production of ketones in the liver. These ketones can then provide the energy needed by the brain.

The researchers found that the low-carb group had improved memory performance whereas the high-carb group experienced no improvement.

This result was even produced at a relatively low average ketone reading of 5.4 mg/dl. This is about 0.5 mMol. Dr.s Phinney and Volek suggest that ketones above 0.5 mMol of concentration in the blood constitute a ketotic state.

The study also found that memory improved as ketone levels increased.

The authors concluded that,

These findings indicate that very low carbohydrate consumption, even in the short-term, can improve memory function in older adults with increased risk for Alzheimer’s disease.

MCT Oil Supplementation Helps In AD

MCT (medium chain triglyceride) oil is a fat harvested from coconut and palm kernel oil. It has the unique ability to pass from the digestive tract right to the liver where it’s metabolized into ketones. These ketones pass into the bloodstream where they can be used for energy by the brain.

These two studies (here & here) found that MCT raised ketone levels sufficiently so that improvements in AD and mild cognitive impairment were observed. The best results occurred with higher ketone levels.

However, there’s a caveat to these studies. Both studies found that individuals with the ApoE4 gene did not fare as well as those without it. This could be because both studies did not control for a low-carb diet and were only interested in MCT results.

Remember, as I mentioned in the risk factors above, individuals with the ApoE4 gene do much better on a low-carb diet than a high-carb one.

Coconut Oil

Coconut oil contains about 60% MCT oil. The consumption of coconut oil should, therefore, produce some increase in ketone levels in the bloodstream.

Watch this to see a remarkable video on how Dr. Mary Newport treated her husband’s Alzheimer’s condition. The remission of his symptoms was astounding.

Interestingly, even though Mr. Newport was ApoE4 positive and not on a low-carb diet, he still experienced significant improvement from coconut oil alone.

As time went on, Mr. Newport was enrolled in a study that tested a relatively new medical food called a ketone ester. This improved his condition even more.

Ketone Salts And Esters

Ketone salts are precursors to ketones manufactured in a lab. When taken orally, they raise ketones in the blood quickly and to a high level (approx 6 mMol). They can be purchased commercially, but there has been some controversy concerning their use.

Ketone esters are also manufactured in a lab and they can also raise ketones quickly.

This study, which included Mr. Newport alone, showed that ketone esters can produce significant improvement in AD patients.

Since ketone esters are still relatively new products, there are still some questions concerning their use in the general public. They’re quite expensive, and users say the taste is absolutely horrible.

For more information on ketone esters, listen to this podcast with Dr. Ben Greenfield and Dr. Richard Veech here. Dr. Veech was the doctor who administered ketone esters to Mr. Davenport.

Note that while MCT oil and exogenous ketones like ketone esters can create ketosis, in order to be effective they have to be constantly administered. A keto diet, on the other hand, will cause ketones to be constantly produced.

However, a keto diet may not raise ketone levels to the degree exogenous ketones will. But unless you’re treating an active disease, this may not be necessary.

The Bottom Line

Back to Barbara. 🙂

Well, we covered a lot here. A ketogenic diet can cause rapid weight loss and be healthy at the same time. In a future post, I’ll describe how I lost 23 pounds in a few months on the keto diet.

In the treatment of AD, research has confirmed that creating ketosis through a keto diet, MCT oil, or ketone esters is an important therapy. And ketosis is also being used to treat Parkinson’s, epilepsy, and many other diseases.

If you have a family history of AD or have the ApoE4 gene or some of the other risk factors, then going keto could be an important preventative tool.

I don’t know if I’m ApoE4 positive. I asked my doctor to do the test, but she didn’t do it. She didn’t think it was necessary. Not necessary? I have a family history of AD and diabetes. And if I have the ApoE4 gene it could increase my chances of AD by 15 times. It’s a constant battle trying to educate our physicians (remember, I had to demand a HbA1c be done). Next time I’ll demand an ApoE4 test.

To guard against AD and to continue to lower my HbA1c, I try to keep my daily intake of net carbs to less than 30 net grams. Am I in ketosis every day? I don’t know for sure, but it’s not necessary to check ketones at this point. However, my blood did test positive for ketones.

So there you have it. What do you think? I encourage you to join in the conversation. Comments are awesome 🙂  In our next post, John will share why he went keto. Then we’ll show you how we’re doing it.

P. S. If you’re looking for low-carb recipes, get a copy of my newly released eBook Bursting With Flavor: 50 low-carb and gluten-free recipes designed to delight your taste buds. This isn’t just any cookbook. It’s filled with my tastiest and healthiest recipes. You’ll be able to walk into your kitchen excited to easily cook a new meal each day.