Tuesday, January 30, 2018

Low-Carb Creamed Spinach

Creamed spinach is the perfect low-carb side to go with pork chops, roast chicken or fish. This recipe is one of my favourite sides included as part of a complete meal in my upcoming Beginner's KetoDiet Cookbook that will be out in April 2018 and is available to preorder!

Spinach is not just low in carbs - it's one of the most nutrient-dense keto foods you can have. It's a great source of vital nutrients such as magnesium, potassium and vitamin A. Also, spinach contains compounds that induce satiety and suppress hunger so you will feel full for longer. Both taste wise and diet wise, this side is a win-win.

To see how easy it is to make it, check out this quick video recipe by our talented recipe developer Lauren!

Preparation time
Hands-on:    15 minutes
Overall:     15 minutes
Nutritional values (per serving)
Total Carbs 8.2 grams
Fiber 4.4 grams
Net Carbs 3.7 grams
Protein 10.9 grams
Fat 20.5 grams
of which Saturated 13.3 grams
Energy 248 kcal
Magnesium 163 mg (41% RDA)
Potassium 1,133 mg (57% EMR)

Macronutrient ratio: Calories from carbs (6%), protein (18%), fat (76%)

Ingredients (makes 3 servings)
  • 600 g fresh spinach (1.3 lb)
  • 2 tbsp butter or ghee (28 g/ 1 oz)
  • ⅓ cup mascarpone cheese (80 g/ 2.8 oz)
  • salt and pepper, to taste
  • ¼ tsp nutmeg
  • ⅓ cup grated Parmesan (30 g/ 1.1 oz)
Instructions
  1. Bring a large pot of water to a boil. Blanch the spinach for 30 to 60 seconds. Immediately plunge the spinach into a bowl filled with ice water.
  2. Drain well, pat dry, and set aside.
  3. Place the butter and mascarpone in a saucepan, and add the blanched spinach and combine.
  4. Add salt, pepper to taste and nutmeg. Gently heat until it begins to simmer.
  5. Then mix in the Parmesan.
  6. Serve topped with more grated Parmesan. Optionally, you can place under the broiler for 2 to 3 minutes, until crisp and lightly golden.
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Monday, January 29, 2018

Low-Carb Butternut Squash Lasagna

Comfort food doesn't get more classic than lasagne. My low-carb and gluten-free take on this Italian classic features delicious layers of thinly sliced butternut squash, homemade marinara sauce, ground beef, creamy herb-infused ricotta, melty mozzarella and crispy Parmesan.

I used pre-cut butternut squash from a local grocery store. If you can get pre-cut squash, it will save you a ton of time but if not, simply use a mandolin.

Although this grain-free lasagna is not ultra low in carbs, it can be included on a keto diet as long as you stay within your macros. It's high in nutrients and ideal for intermittent fasting when you eat one or two meals per day.

Preparation time
Hands-on:    20 minutes
Overall:     1 hour 15 minutes
Nutritional values (per serving)
Total Carbs 15.4 grams
Fiber 2.3 grams
Net Carbs 13.1 grams
Protein 45.3 grams
Fat 56 grams
of which Saturated 24.3 grams
Energy 747 kcal
Magnesium 74 mg (19% RDA)
Potassium 805 mg (40% EMR)

Macronutrient ratio: Calories from carbs (7%), protein (25%), fat (68%)

Ingredients (makes 6 servings) Instructions
  1. Prepare the Marinara Sauce by following this recipe. Preheat the oven to 200 C/ 400 F.
  2. I used pre-cut butternut squash lasagne sheets. If you can't get pre-cut slices, simply peel the butternut squash and remove the seeds. Then use a mandolin to slice it thinly (about ⅛ inch or ¼ cm).
  3. Grease a large pan with ghee and add the ground beef. Cook for 5-7 minutes while stirring, or until opaque. Add half of the marinara sauce and oregano. Season with half of the salt and pepper.
  4. Prepare the ricotta layer. Combine the ricotta, eggs, chopped parsley and basil. Season with the remaining salt and pepper.
  5. Spread the remaining marinara sauce on the bottom of a large casserole dish. I used a 26 x 18 x 6.5 cm (10 x 7 x 2.5 inch) casserole dish. Add the first layer of butternut squash slices. You will use a total of 3 butternut squash layers.
  6. Top with half of the ground meat mixture and half of the ricotta cheese mixture.
  7. Add another layer of butternut squash slices and top with the remaining ground beef.
  8. Spread the remaining ricotta cheese mixture on top of the ground beef.
  9. Top with the remaining butternut slices, grated mozzarella and Parmesan cheese.
  10. Cover the casserole with a baking foil and transfer into the oven. Bake for 45 minutes. Remove the foil and bake for 7-10 minutes.
  11. Remove the lasagna from the oven and let it rest for 15 minutes before slicing. Once cooled, it can be stored in the fridge for up to 4 days.
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Sunday, January 28, 2018

The Ketogenic Diet for Alzheimer's Disease

In part 1 of this look at Alzheimer's disease (AD), I introduced the concept of Alzheimer's as a metabolic condition. The primary driver of the disease pathology, and what's mainly responsible for the memory loss, cognitive impairment, personality changes and other signs and symptoms, is that neurons in affected regions of the brain become unable to effectively metabolize glucose.

Since, under normal circumstances, glucose is the brain's primary fuel, when neurons lose the ability to metabolize it, they essentially starve. And remember, the brain needs a large and constant supply of energy—even when you're just lying around watching TV or sleeping, when you think your brain isn't doing much, it's still using lots of energy.

I left off in part 1 emphasizing that the energy shortage in the brain is specific to glucose, and proposing that it would be possible to nourish these starving cells if there were some type of alternative fuel they could use. One of the bright spots in the darkness that is Alzheimer's disease is that these struggling, atrophied neurons can still metabolize ketones!

"When glucose utilization is impaired in neurodegenerative diseases, transport of KBs [ketone bodies] into the brain appears to be less affected and their utilization for energy by the brain mitochondria is not impeded by such factors as local insulin resistance that, by interfering with the neuronal fuel supply, may contribute to the progressive nerve cell damage observed in Alzheimer's disease" (1).

Ketones as Brain Fuel

Under certain circumstances, ketones can provide as much as 60% of the brain's energy (1). It may be that such a large portion of the brain's energy needs can only be met by ketones when ketone levels are relatively high—higher, perhaps, than most people would be able to achieve through a ketogenic diet alone.

But while the brain's use of glucose is compromised, it's not completely destroyed. Some glucose is still metabolized, so even if ketones only contribute a small amount of available energy, it's still a boost to cognitive function.

Do Ketone Levels Matter?

Uptake of ketones into the brain is directly proportional to the blood concentration of beta-hydroxybutyrate (βOHB) and acetoacetate: the higher the ketones, the more the brain will take them in.

During a prolonged fast, serum βOHB levels can reach 5-7 mmol/L (1). At a βOHB concentration of 1.5 mM, ketones supply about 18% of the brain's energy; 60% is achievable at 6 mM (2). However, people vary in the level of ketones they might respond to. Some people might notice improved cognition with relatively low ketones, while others will need to get their ketones elevated higher in order to experience a benefit for the brain.

Elevating Ketones is Beneficial for Alzheimer's

Elevated ketones clearly reduce the amount of glucose the brain requires. It would be difficult for an older individual to achieve a ketone level of 6 mM with a ketogenic diet alone, but a KD in conjunction with exogenous ketones or additional MCT oil could provide the brain with a substantial fuel supply.

The Evidence

Fortunately, we don't have to rely solely on mouse models and petri dish studies to assess whether ketones can be beneficial for people with AD or its precursor, mild cognitive impairment (MCI), although that evidence exists, and it's promising (3).

Several studies in human subjects with AD have shown that elevated ketones do lead to improved cognition. Many such studies have employed exogenous ketones, but some have used medium-chain triglyceride (MCT) oil or a ketogenic diet, and there's evidence that all three approaches can be effective.

The Ketogenic Diet without Ketone Supplementation

In a small study of adults with MCI, six weeks of following a ketogenic diet (~34g carbs per day) resulted in significant decreases in body weight waist circumference, fasting glucose, and fasting insulin. The reduced insulin had a small correlation with improved memory (4). The authors wrote:

"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. While this effect may be attributable in part to correction of hyperinsulinemia, other mechanisms associated with ketosis such as reduced inflammation and enhanced energy metabolism also may have contributed to improved neurocognitive function" (4).

MCT Supplementation

In a different study of subjects with AD or MCI, subjects following a standard diet consumed a beverage containing emulsified MCTs, and then they completed some of the formal assessments for AD. In subjects without the ApoE4 gene, compared to placebo, the MCT drink resulted in improved scores on the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog) (5). Subjects with the ApoE4 gene improved only in one test, for paragraph recall. (In all subjects, regardless of ApoE genotype, higher ketones correlated with better recall.)

As I explained in part 1, carriers of the E4 gene are likely the least suited to the modern high-carb diet. With this in mind, it may be that elevating their ketone levels via one-time MCT administration is not sufficient to improve cognition in an acute setting. We'll look at MCT oil and exogenous ketones in more detail in a bit. Before leaving this study, though, it's important to note that the MCT treatment resulted in a mean βOHB level of only 0.5 mmol/L. This isn't all that high.

According to well-known low carb researchers Stephen Phinney and Jeff Volek, 0.5 mM is the very bottom of the cutoff for nutritional ketosis (0.5-5.0 mM) (6), so it's possible that subjects would have had even better improvement in cognitive assessments if their ketone levels were higher.

A separate study of an MCT oil preparation had similar but more promising findings. In subjects with mild-to-moderate Alzheimer's, compared to placebo, daily consumption of the MCTs for 90 days resulted in significant improvements in multiple cognitive assessments, with improvements being greatest in non-ApoE4s who were compliant with dosing (7). ApoE4 gene carriers showed no significant improvements.

The Limitations of Studies Involving Ketone Supplements

A major flaw of this study is that subjects were advised to mix the packets they were given (either the MCT or placebo) in 8 ounces of water, juice or milk. As if that weren't bad enough, to increase compliance and palatability, they were later recommended to mix them into Ensure™, which is notoriously loaded with sugar! Taking this into account, it's heartening they showed any cognitive improvement at all!

This is a major flaw of almost all studies involving MCTs and exogenous ketones, actually: these compounds are typically added to subjects' habitual diets, which are usually a standard Western or American diet, high in refined carbs and omega-6-rich seed oils.

That we see any improvement solely from slightly elevated ketones is encouraging. It shouldn't surprise us that some people with Alzheimer's don't show improvement with no other intervention besides elevated ketones; what should surprise us is that so many do.

Can Ketones Help ApoE4s?

It's true that most of the studies looking at MCTs for Alzheimer's show more favorable results for non-ApoE4s than for E4s. People with the E4 gene, however, do experience improved cognition under certain circumstances.

The most encouraging example of this was Mr. Steve Newport, husband of Mary Newport, MD, author of The Coconut Oil and Low-Carb Solution for Alzheimer's, Parkinson's, and Other Diseases (8). Mr. Newport was an ApoE4 carrier, and he experienced rapid and dramatic improvements in several aspects of cognitive function and performance of tasks for everyday living after being treated first with coconut oil and later with a ketone ester (9).

When Dr. Newport first became aware of the research on ketones for brain health and cognitive function, she added coconut oil to her husband's morning oatmeal. With just that small change—adding coconut oil to a high-carbohydrate diet-she noticed enough of an improvement to continue, increase the dose over time, and eventually progress to using a ketone ester, still in the context of a relatively high-carb diet. The ketone ester allowed Mr. Newport to experience βOHB levels as high as 7.0 mM (9).

The dramatic elevation of ketones resulted in him being able to perform tasks he had been unable to perform unaided for several months, such as shaving and showering. As improvements continued, he was able to perform more complex tasks, such as yardwork and other household chores, as well as "spontaneously discussing events that occurred up to a week earlier." Abstract thinking and his sense of humor returned, and he self-reported feeling well, having more energy, feeling happier, and finding it "easier to do things"-all of which Dr. Newport's observations corroborated (9).

Sadly, Mr. Newport lost his battle with Alzheimer's in January 2016, but his quality of life and that of his loved ones and caregivers were improved by his substantially improved cognitive function owing to their experiments with regularly elevated ketones. (You can watch Dr. Newport's fascinating account of her husband's remarkable improvement with ketone treatment here.)

ApoE4 May Need More Than Ketone Supplements

Recall from part 1 that people with the ApoE4 gene are believed to be the least suited for the modern high-carb diet. If this is true, then it's no surprise that most E4 carriers show little to no improvement from interventions that elevate ketones a single time in a laboratory, or even from interventions that elevate ketones for an extended period of time but do nothing else, especially when this happens in the context of the usual high-carb diet.

If the E4 gene is a product of the hunter-gatherer environment, then elevated ketones, by themselves, might not be enough to have a noticeable impact on cognition in E4s with Alzheimer's. It may be that E4s have to adopt several other changes that would help restore their metabolism and hormonal milieu to something more befitting them, including better quality and quantity of sleep, stress reduction, increased physical activity, fasting, and repletion of vitamins and minerals they may be deficient in.

"A modified 'Paleolithic prescription' may prevent AD. The Paleolithic prescription proposes a change in diet and activity to a level more similar to our Late Paleolithic ancestors. […] Therefore, reducing dietary intake of high-glycemic carbohydrates and increasing protein, fiber and fat would be preferred. Similar diets appear to reduce the risk of AD. Since HC [high carb] diets are proposed to be the primary cause of AD regardless of apoE genotype, such a diet would generally reduce the risk of AD. However, this diet is predicted to be particularly beneficial to carriers of apoE4." (10)

Individuals with the ApoE4 gene are having remarkable success using a mild ketogenic diet and multifactorial lifestyle intervention protocol created by Dale Bredesen, MD, and outlined in his book, The End of Alzheimer's (11).

Ketogenic Diet Versus Exogenous Ketones

Raising ketone levels via coconut oil, MCT oil, or exogenous ketones can be a gift to those suffering from Alzheimer's. Elevated ketones have clearly been shown to result in improved cognition; however, this is a short-term fix.

It's putting a band-aid on a sucking chest wound. Ketones are metabolized fairly rapidly; once they're gone from the bloodstream, so are their beneficial effects. For elderly people, or people with very advanced and severe dementia, exogenous ketones can still have a powerful acute effect. But contrast this with a ketogenic diet, which would have someone generating endogenous ketones all the time.

Not only would a ketogenic diet help someone have elevated ketones around the clock, instead of only after using exogenous ketones, but the KD also induces a host of other effects that exogenous ketones can't mimic.

Ketogenic diets are anti-inflammatory, they reduce glucose and insulin levels, reduce formation of reactive oxygen species ("free radicals"), may help increase mitochondrial biogenesis (making new mitochondria), enhance glutathione levels in the brain, and more (12,13,14).

By providing βOHB to fuel languishing neurons, exogenous ketones help make up for the glucose fuel deficit, and we shouldn't downplay the significance of this, but they don't result in any of the other long-term benefits of the KD. For the purpose of improving cognitive function in AD, elevating ketones is probably the most important step, but it's not the only one. The diet has several effects that can't be mimicked solely by exogenous ketones or ketones induced via MCT oil. It would be a major blockbuster, but as of yet, there is no "ketogenic diet in a pill" (14).

Bottom line: exogenous ketones are an adjunct to, not a substitute for, a ketogenic diet. But for those of very advanced age or with severe impairment, who can't or won't change their diet, exogenous ketones are worth trying.

Special Considerations on the Ketogenic Diet for Alzheimer's

In order to help a loved one implement a ketogenic diet, you have to have complete control over their diet. It will be virtually impossible if the afflicted individual lives in a care facility where their food is provided for them. In situations where supportive family members and friends can help with food shopping and meal preparation, the younger someone is, and the more mild their degree of cognitive impairment, the more likely they are to experience improvements from a ketogenic diet, and the easier it will be to implement one.

The older an individual, and the more severe their impairment, the more difficult it will be to change their diet. People with advanced Alzheimer's may be belligerent and uncooperative, making it almost impossible to have them adhere to a KD. Big changes in diet can be difficult enough when we want to change; forcing a change upon someone who does not want it is an exercise in frustration and futility.

Alzheimer's disease is striking people at ever younger ages, but it still primarily strikes those who are older. With that in mind, here are some things to consider when implementing a KD for improving cognitive function:

Digestive Fire Naturally Decreases with Age

The increase in fat, and, for some people, protein, might take some getting used to for someone accustomed to living on cereal, pasta, bread, and fruit. In order to get the best benefits from a KD, older people may need digestive support in the form of supplemental HCl (betaine HCl), ox bile, or digestive enzymes, all of which are available online or at health food stores.

Many Older Individuals are Underweight

For those in this category, be sure they're getting enough calories. Protein should not be restricted in the underweight, and fasting is not recommended. Higher ketones can be achieved with liberal intake of coconut or MCT oil, rather than with fasting or limiting protein.

Some Drugs May Hinder Progress

Certain pharmaceutical drugs common among older people may hinder progress. Statin drugs and prescription antacids are two of the most common. Work with a physician to see if it is prudent to continue the medication or if they can be discontinued. (Remember: 25% of all the body's cholesterol is in the brain! You cannot have healthy cognitive function without adequate cholesterol. Regarding antacids, what's the point of someone eating a nutrient-dense, cognition-supporting diet if they also take a drug that impairs healthy digestion and absorption of those nutrients?)

Emotional Support is Crucial

People of all ages can benefit from having a "diet buddy" - someone else in the same household who will follow a ketogenic diet along with them, or perhaps do a slightly more liberal variation of a low-carb diet.

Don't underestimate the importance of emotional support and solidarity; this can make adhering to the diet easier. Considering the myriad issues these ways of eating are beneficial for, the whole family can be involved. Even for those with no known health issues and who are not overweight, no one's health ever got worse from eliminating refined sugar and processed food from their diet.

Take Home Message: There is Hope

The ketogenic diet is not a slam dunk for Alzheimer's. There are still unanswered questions, and much research remains to be done. But considering there are no effective pharmaceuticals and no effective alternatives for people living with AD, keto may be worth trying.

That people with mild cognitive impairment and Alzheimer's Disease do show improved cognition when ketones are elevated is proof that their withering, atrophied neurons aren't dead; they're hibernating. It's as if they're in "powersave mode," downregulating non-essential functions to conserve energy until they receive enough fuel to bring everything back online. According to Alzheimer's researcher Stephen Cunnane and colleagues:

The brain energy deficit in Alzheimer's "can at least in part be bypassed by ketogenic treatments. A core element of this interpretation is that brain cells and/or networks that were previously dysfunctional can start to function more normally again once they are provided with more fuel, i.e., they were starving or exhausting but not dead; otherwise this cognitive improvement would not be possible" (15).

If the primary pathological feature of Alzheimer's disease is reduced glucose usage in the brain, then the logical first step is to provide the brain with an alternative fuel, in the form of ketones.

If you'd like to learn more about Alzheimer's disease as "type 3 diabetes" and the potential therapeutic use of ketones and the ketogenic diet, consider exploring my book, The Alzheimer's Antidote: Using a Low-Carb, High-Fat Diet to Fight Alzheimer's Disease, Memory Loss, and Cognitive Decline.

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Saturday, January 27, 2018

Keto Chipotle Prawn & Broccoli Salad

It's a common misconception that keto is just about bacon, eggs and cheese. In reality, there is a variety of foods you should eat to get all the nutrients you need. For this salad I used a few simple ingredients. The dressing is full of smokey flavour - not too spicy and with a nice hint of lime.

Preparation time
Hands-on:    10 minutes
Overall:     15 minutes
Nutritional values (per serving)
Total Carbs 12.6 grams
Fiber 4.1 grams
Net Carbs 8.5 grams
Protein 29.2 grams
Fat 38.2 grams
of which Saturated 5.3 grams
Energy 509 kcal
Magnesium 84 mg (21% RDA)
Potassium 786 mg (39% EMR)

Macronutrient ratio: Calories from carbs (7%), protein (24%), fat (69%)

Ingredients (makes 2 servings) Dressing: Salad:
  • 250 g cooked prawns or shrimp (8.8 oz)
  • ½ medium broccoli, cut in florets (200 g/ 7.1 oz)
  • ½ medium red bell pepper, sliced (60 g/ 2.1 oz)
  • ½ small red onion, sliced (30 g/ 1.1 oz)
  • 4 cups mixed leafy greens of choice (120 g/ 4.2 oz)
  • 1 tbsp chopped cilantro or parsley
Instructions
  1. Prepare the dressing by mixing the mayonnaise, olive oil, and lime juice. Season with salt and pepper to taste.
  2. Place the cooked prawns in a bowl, add half of the dressing and combine well. Keep the remaining dressing for later.
  3. Steam or boil the broccoli florets until crisp tender, for 5-7 minutes. Then, place the cooked broccoli in ice water to quickly cool down. Drain and set aside.
  4. Slice the red pepper and onion. Assemble the salad by dividing the ingredients between 2 bowls.
  5. Start with the greens, add the cooked broccoli florets (cut in smaller pieces if needed), sliced red pepper and sliced onion. Top with the dressed prawns and drizzle with the remaining dressing. Finish by adding chopped cilantro and cracked black pepper.
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Thursday, January 25, 2018

Squash Casserole

An easy and simple keto friendly squash casserole! Only 4 ingredients! Check out more keto friendly -> RECIPES http://ift.tt/2Fdfvxy

Wednesday, January 24, 2018

Quick & Easy Cucumber Radish Salad

This keto salad is based on an old classic - creamy cucumber salad. What I love about it most is that it takes just a few minutes to prepare and uses a few simple ingredients.

Unlike the traditional recipe which includes sour cream, I made it dairy-free by using paleo mayonnaise and added sliced radishes for an extra crunch. I like to serve mine as a side with steak, barbecued fish, or crispy duck breast.

Preparation time
Hands-on:    10 minutes
Overall:     10 minutes
Nutritional values (per serving)
Total Carbs 6.1 grams
Fiber 1.8 grams
Net Carbs 4.2 grams
Protein 1.7 grams
Fat 23.2 grams
of which Saturated 3.3 grams
Energy 234 kcal
Magnesium 23 mg (6% RDA)
Potassium 324 mg (16% EMR)

Macronutrient ratio: Calories from carbs (7%), protein (3%), fat (90%)

Ingredients (makes 6 servings) Dressing: Salad:
  • 3 large cucumbers, sliced (900 g/ 1 lb)
  • 200 g radishes, sliced (7.1 oz)
  • ½ large red onion, sliced (85 g/ 3 oz)
Instructions
  1. Prepare the dressing by mixing the lemon juice and mayonnaise.
  2. Season with salt and pepper to taste. Optionally, add 1-2 teaspoons of vinegar. Add freshly chopped dill and mix well.
  3. Using the slicing attachment on your food processor or a knife, thinly slice the cucumbers, radishes, ... ... and red onion. Place the sliced vegetables in a mixing bowl.
  4. Pour the prepared dressing over the sliced vegetables.
  5. Mix until well combined. Serve as a side with meat or fish, as an appetiser, or light dinner. Eat immediately, or store in the fridge for up to 2 days.
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Tuesday, January 23, 2018

Parmesan Roasted Acorn Squash

An easy to make dinner perfect for winter! Break out that acorn squash and get cooking! Check out more ketogenic -> RECIPES http://ift.tt/2BmWaaI

Is Alzheimer's a Metabolic Disease?

Whether you’re new to a ketogenic diet or have been following one for a while, you’ve probably heard this way of eating is beneficial for fat loss, diabetes (both type 2 and type 1), metabolic syndrome, PCOS, and more.

But what might come as a surprise is that this low-carb, high-fat way of eating is a promising nutritional intervention for a condition for which there are no effective treatments: Alzheimer’s disease.

What is Alzheimer’s Disease?

Alzheimer’s disease (AD) tops the list people’s most feared illnesses, and for good reason. Except for generally striking people of older age, Alzheimer’s seems to strike indiscriminately. AD affects people of all ethnicities, races, nationalities, faiths, and genders. There’s only one kind thing we can say about AD, and it’s that it doesn’t discriminate: Alzheimer’s is an equal opportunity killer.

However, even though Alzheimer’s disease typically strikes people later in life, it’s no longer a condition that exclusively afflicts elderly people. With a play on words, they used to casually call Alzheimer’s disease “Old Timer’s Disease.” But we’re not talking only about elderly people anymore. AD now affects people ever younger; individuals in their 50s and 60s are being diagnosed with early-onset Alzheimer’s, or the precursor to AD, called “mild cognitive impairment” (MCI). Why is this happening? Why is this frightening form of dementia increasing in incidence, and affecting people at younger ages?

Alzheimer’s is a Metabolic Condition

When it comes to conditions such as cardiovascular disease, obesity, type 2 diabetes, infertility, and more, we take it for granted that diet and lifestyle play a role, if not the primary role. No one even questions this anymore.

But for some reason, when it comes to Alzheimer’s, we believe we’re clueless. We feel like we have no idea where it’s coming from, while ignoring the possibility that it might be driven by the same factors behind so many other chronic modern diseases: diets and lifestyles that are a mismatch for healthy human physiology.

In scientific journals, Alzheimer’s disease is regularly referred to as “type 3 diabetes” or “brain insulin resistance” (1, 2). Without knowing anything else about the condition, these phrases immediately hint that there’s a connection to glucose and/or insulin in the brain.

Indeed, the primary problem in the Alzheimer’s brain is that neurons in affected regions have lost the capacity to get energy from glucose. Ultimately, Alzheimer’s disease is a metabolic problem; that is, it has to do with the way the brain generates and uses energy.

This condition is complex and multifactorial, but at its heart, AD is an energy crisis in the brain. A fuel shortage. And the brain is an energy hog — it needs constant fuel, and lots of it. The brain accounts for just 2% of a typical adult’s body weight, but it consumes 20-25% of the body’s glucose and oxygen. With such high energy requirements, any disruption in fuel supply to areas responsible for memory processing, learning, and behavior would have catastrophic consequences for cognitive function:

“Given the high energy requirement of the brain and its critical dependence on the delivery of a constant supply of fuel, the consequences of leaving such an energy shortfall untreated can be dire. When the brain’s energy supply is insufficient to meet its metabolic needs, the neurons that work hardest, especially those concerned with memory and cognition, are among the first to exhibit functional incapacity (e.g., impairment of memory and cognitive performance)” (3).

In keeping with the idea that AD is a brain energy shortage, think about what happens when you’re tired. You get clumsy, right? You move more slowly, and you make mistakes you wouldn’t normally make. Well, what happens when the brain gets tired? It, too, gets clumsy, sluggish, and starts making mistakes. And considering just how much energy the brain needs every second of every day — even when we’re asleep — anything that interferes with fuel use in the brain will have a negative impact on cognition.

What is a Neuron and How Does it Work?

Here’s a simplified look at the basic structure of a neuron:

The way neurons communicate with each other is that neurotransmitters and other chemical messages are broadcast out the axon terminals of one neuron and received at the dendrites of other neurons, like a radio station broadcasting a signal. But axon terminals and dendrites don’t actually touch. There’s a tiny bit of space between them, called a synapse, and this is where the communication happens.

When a neuron is not receiving or using adequate fuel, in order to conserve energy to keep the cell body alive (the main part of the cell), the neuron sucks the axons and dendrites back in toward the cell body, like a vacuum with a retractable cord.

When the axons and dendrites recede back toward the cell body, the synapse is no longer viable; the space is too big for proper communication to occur. Memory loss and cognitive impairment are the logical outcomes of this. The receding of these crucial structures can be seen via MRI scan (magnetic resonance imaging): doctors can actually see that the physical volume of the brain has shrunk.

Alzheimer’s Takes Years or Even Decades to Develop

The rate at which the brain uses glucose is called the cerebral metabolic rate of glucose (CMRglu). Alzheimer’s patients may have up to a 45% reduction in CMRglu. Reduced brain glucose usage is a universal feature of AD, and some researchers have called this the predominant abnormality in the condition (4). A key point here is that this decrease in CMRglu can be measured in people at risk for AD as young as their 30s and 40s (5).

Alzheimer’s doesn’t develop overnight. No one wakes up “all of a sudden” with severe AD. Reduced brain glucose metabolism is one of the earliest steps in the disease process, if not the earliest step. However, even if someone in their 30s or 40s is already experiencing a decline in CMRglu, they typically don’t show any signs or symptoms of dementia. At that age, they’re still young and robust, and the brain is able to compensate.

Signs and symptoms only emerge when a tipping point has been reached where the “fuel crisis” has been going on for so long, and the resulting damage is so widespread, that the brain can no longer make up for it. But it’s important to understand that signs and symptoms emerge relatively late in the disease process; by the time cognitive problems are noticeable, the pathology has been in place for years, maybe decades (6, 7).

This may be part of why the illness has proven so difficult to treat. That damage often accrues silently for so long is also why putting efforts toward potential prevention is so crucial, rather than focusing solely on slowing or stopping the decline once it’s already begun.

What are the Risk Factors for Alzheimer’s Disease? Advanced Age

Obviously, one of the primary risk factors for developing AD is advanced age. According to the Alzheimer’s Association:

“Of the estimated 5.5 million Americans living with Alzheimer's dementia in 2017, an estimated 5.3 million are age 65 and older and approximately 200,000 individuals are under age 65 and have younger-onset Alzheimer's.”

AD is the sixth leading cause of death in the U.S., and the fifth leading cause of death among people age 65 or older. However, keep in mind that, as I’ve mentioned, it’s likely that the disease only becomes apparent at this older age. The pathological problems driving the disease begin in much younger years.

ApoE4 Gene

Aside from advanced age, there are multiple risk factors for AD. One of the strongest is the ApoE4 gene. This is even sometimes called “the Alzheimer’s gene,” but this is misleading (8).

We have two copies of each gene, one from our mother and one from our father. And it’s true that having one copy of the ApoE4 gene increases risk for AD, and having two copies increases it even more. But not everyone with two copies develops Alzheimer’s, and many people who are afflicted with Alzheimer’s do not carry even one copy! So, this gene is neither required, nor sufficient, to cause AD (9).

This being the case, why does ApoE4 increase risk so much?

Like so many modern chronic illnesses that have reached epidemic proportions, Alzheimer’s disease seems to be a mismatch between our evolutionary conditioning and our current diet and lifestyle (10, 11).

The ApoE4 gene is strong evidence for this. E4 is believed to be the oldest form of the ApoE gene. (The two other forms of ApoE in humans are E2 and E3.) It’s hypothesized that the E4 variant was forged during our hunter-gatherer times, and it has been selected against in populations with a longer history of grain-based agriculture (11, 12).

In other words, human populations with a longer history of consuming grains — that is, a higher carbohydrate diet — have a lower incidence of this gene. So it’s not that the E4 gene, by itself, is harmful. What it means is, people who carry the E4 gene are not well-suited for a high-carb diet, and thus, they suffer the greatest metabolic damage when faced with the modern diet, which is awash in refined sugars and grains.

According to prominent Alzheimer’s researcher Sam Henderson (11):

“It should be noted that E4 is not an inherently damaging allele; it is only deleterious in combination with a HC [high-carb] diet (which is deleterious on its own).”

Chronically Elevated Insulin

Beyond genetics, a powerful risk factor for developing AD is chronically elevated insulin, also called hyperinsulinemia. Even for people whose blood glucose is normal, if insulin is chronically elevated, risk is greater for developing AD. (13, 14, 15, 16)

For this reason, the phrase “type 3 diabetes” is a bit misleading. Type 2 diabetes is diagnosed solely through glucose measurements, but with regard to AD, it’s not always high glucose causing the problem, but rather, high insulin. The reason this important risk factor is missed in so many people is simply that insulin testing is not a standard part of routine bloodwork, the way fasting blood glucose measurements are.

Even hemoglobin A1c, which is taken to represent a 3-4 month average of blood glucose levels, has become commonplace, but insulin is still rarely measured. If insulin tests were included in routine checkups, people at risk for disorders associated with insulin resistance—such as gout (17), hypertension (18), PCOS (19), benign prostate hyperplasia (BPH) (20), and Alzheimer’s — could be identified long before these conditions take root and cause years of worsened health and reduced quality of life.

“Insulin resistance is usually at or near the top of the list of known lifestyle-related factors heightening the risk of declining cognition in the elderly” (21).

“An emerging body of evidence suggests that an increased prevalence of insulin abnormalities and insulin resistance in Alzheimer’s disease may contribute to the disease pathophysiology and clinical symptoms” (22).

What is the Role of Beta-Amyloid in AD?

If someone in your life is afflicted with Alzheimer’s, or you’re interested in AD research, you’ve no doubt come across the terms beta-amyloid, or amyloid plaques. Amyloid plaques are frequently cited as the cause of Alzheimer’s, but there are problems with this theory. First, though, what is beta-amyloid, and what does it do?

Beta-amyloid (Aβ) is a protein secreted by neurons in response to injury, be it biochemical injury, as in Alzheimer’s, or physical trauma, as is observed in traumatic brain injury (22, 23). When these initially protective protein fragments are cleared away efficiently, they’re not a problem. But when they’re left to accumulate — as if the cleanup crew that’s supposed to sweep them away is on strike — they bind to each other and form “plaques.” These plaques block the synapses between neurons, ultimately interfering with neuronal communication. When neurons can’t send signals back and forth, the logical results are declining cognition, memory loss, behavioral changes, and the other problems we observe in AD.

Are Amyloid Plaques the Cause of AD?

So it seems logical that these amyloid plaques could be causing Alzheimer’s. However, many people who lose their lives to AD do not have extensive plaque deposition in the brain, and plenty of people who die from other causes are found upon autopsy to have significant plaque deposition (24). Plus, the plaques tend to appear late in the disease process. The first domino to fall — the earliest step in the pathology — is the reduction in the brain’s glucose metabolism. The plaques come much later. Amyloid plaques might be exacerbating cognitive impairment, but they’re not the initial cause.

“A prominent and well-characterized feature of AD is progressive, region-specific declines in the cerebral metabolic rate of glucose (CMRglc) […] Carriers of a common Alzheimer’s susceptibility gene [APOE Ɛ4] have functional brain abnormalities in young adulthood, several decades before possible onset of dementia. Therefore, low regional CMRglc 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” (29).

Why Amyloid Proteins Are Neuroprotective

Additionally, amyloid proteins are neuroprotective. They have numerous functions that suggest they play a vital role in neuronal repair and regeneration (22). If they were contributing to the disease pathology, then we would expect a drug that reduced secretion of these proteins and formation of the plaques to have a beneficial impact on the illness.

It is noteworthy, then, that every drug developed to target these proteins and plaques has been a failure. They’ve succeeded in that they did reduce secretion of amyloid proteins and plaque formation, but these reductions led to no improvement in the condition. In fact, phase III clinical trials of one such drug were stopped early because in subjects on the drug, cognitive function was declining so much faster than in those on the placebo, and it would have been unethical to continue (25).

The amyloid proteins are initially protective, but it’s true that when they form into plaques, things can go awry. Think of it like a fever: a fever is initially a protective step. It’s your body’s way of raising your core temperature in order to fight off a pathogen inside you, like a virus or bacteria. But if the fever goes too high, then the fever, itself, becomes a problem. It’s a similar situation with amyloid proteins. At relatively low levels, they’re helpful. It’s only when they build up and start linking together that they form plaques and interfere with cellular communication.

The Role of Insulin Degrading Enzyme (IDE)

What’s fascinating about this is, what’s responsible for clearing them away — the cleanup crew I mentioned before — is something called insulin degrading enzyme. This is exactly what it sounds like in plain English: it’s the same enzyme that clears away insulin. (Some enzymes in the body have only one job, but others, like IDE, have multiple jobs.)

The key thing to know here is, IDE favors insulin above everything else. So, whenever there’s a significant amount of insulin to be cleared out of the blood, IDE will always be drawn to it first, leaving all its other jobs — like clearing away amyloid—to be done later.

When someone has healthy insulin levels most of the time, this isn’t a problem. But in someone with chronically high insulin — as is the case for so many people these days — the vast majority of IDE’s attention will be on dealing with all the insulin, and as a result, the amyloid is left build up and cause trouble (26, 27).

People With the E4 Gene Produce Less IDE

An interesting tidbit that connects IDE to the ApoE4 gene and the increased risk it confers for AD is that people with the E4 gene produce less IDE than people with other variations of this gene (28).

That’s right: they produce less IDE, perhaps suggesting that, as hunter-gatherers presumably with a much lower carbohydrate intake, they may have produced less insulin, and thus have had less need for the enzyme that degrades it.

Take Home Message

Alzheimer’s disease is not an unknowable mystery. For sure, there are still many unanswered questions and much research remains to be done. But that doesn’t mean we’re completely in the dark about what’s happening inside the Alzheimer’s brain and what to do about it.

To the extent that AD is a metabolic condition, the solution is also a metabolic one: change the way the brain gets energy. Owing to the way a ketogenic diet provides an alternative fuel to the brain—transitioning from dependence on glucose to reliance on ketones—it’s a logical and scientifically sound place to start.

To Be Continued…

If Alzheimer’s disease results primarily from a fuel shortage in the brain — a shortage occurring because affected neurons are no longer able to use glucose effectively — then if there were some kind of alternative fuel that could nourish these starving cells, perhaps we could slow the progression of this illness, or, if caught early enough, potentially even stop it and undo some of the damage. Next time, we’ll explore exciting research that gives us hope in the otherwise vast darkness that surrounds this condition.

Here’s a sneak peek:

“Two points are clear – (i) AD is at least in part exacerbated by (if not actually caused by) chronic, progressive brain fuel starvation due specifically to brain glucose deficit, and (ii) attempting to treat the cognitive deficit early in AD using ketogenic interventions in clinical trials is safe, ethical, and scientifically well-founded” (30).

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Monday, January 22, 2018

Keto Cinnamon Toast Crunch Cereal

Which one of you misses their crispy bowl of breakfast cereal? Maybe just out of habit, convenience or simply because you love cinnamon - just like I do!

This keto cinnamon toast crunch is hands down the best cereal I've had since going low-carb. And as you can see in my new video recipe, it is actually quite easy to make. You can bake a double or triple batch and keep it in an airtight container for up to 2 weeks. Enjoy!

Preparation time
Hands-on:    15 minutes
Overall:     1 hour
Nutritional values (per ⅔ cup/ 57 g/ 2 oz)
Total Carbs 7.9 grams
Fiber 4.4 grams
Net Carbs 3.5 grams
Protein 6.4 grams
Fat 26.6 grams
of which Saturated 8.5 grams
Energy 282 kcal
Magnesium 87 mg (22% RDA)
Potassium 230 mg (12% EMR)

Macronutrient ratio: Calories from carbs (5%), protein (9%), fat (86%)

Ingredients (makes 6 servings) Dough: Topping:
  • 2 tbsp melted butter or ghee, divided (30 ml/ 1 fl oz)
  • 1-2 tsp cinnamon, divided
  • 1-2 tbsp granulated Erythritol or Swerve, divided (10-20 g/ 0.3-0.7 oz)
Instructions
  1. Place all the dry ingredients in a bowl: almond flour, flax meal, baking powder, cinnamon, Erythritol and salt.
  2. Mix well.
  3. Add the melted butter and vanilla extract.
  4. Mix until well combined. Add the water and mix until the dough has formed. Refrigerate for 1 hour.
  5. Place about half of the dough on a silicon mat. Use a silicon lined rolling pin to roll out the dough until very thin, about ⅛-inch (¼ cm). Alternatively, place the dough between 2 sheets of parchment paper and roll out until thin.
  6. Use a pizza cutter to cut the dough into small squares. Using a fork, prick each of the square.
  7. Brush with melted ghee.
  8. Dust with cinnamon and sprinkle with Erythritol. Repeat for the second half of the dough, using the remaining melted butter, cinnamon and Erythritol.
  9. Place in the oven preheated to 300 F/ 150 C and bake for 20 minutes.
  10. Remove from the oven and place on a cooling rack for 1 hour to allow the cereal to crisp up.
  11. Once completely cooled, break the pre-cut cereal into pieces.
  12. Serve with unsweetened almond milk, coconut milk or full-fat yogurt.
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