This month sees the celebration of National Nutrition Month, and so for the next few weeks, I’m going to take a deeper dive into some of the most popular “anti-cancer” diets, with a closer look at the evidence base underlying their potential to protect us against cancer.
This week, let’s start the ball rolling with the ever popular ketogenic diet (or “keto”, for short). I’m pretty sure you’ve definitely heard about this one, and you might even have tried it yourself in a bid to lose weight (Atkins, anyone?!), but with all the talk of different types of diet, it can be difficult to discern the subtle, but significant, differences between them.
So first things first, let’s get clear on what keto is.
Many people think keto and Atkins are the same. Well, almost, but not quite...they ARE the same in the induction phase of Atkins, where participants are required to follow a strictly low carb, high fat diet, but longer term, keto remains low carb, whereas Atkins allows the reintroduction of more carbohydrates and proteins later on.
The ketogenic diet was originally developed in the 1920s to treat unmanageable epilepsy in children, but has since been adopted to help with weight loss and overall health, and more recently, has been touted as a potential “anti-cancer” diet.
Keto follows the principles of eating a high-fat, adequate-protein and low-carbohydrate diet (c. 70% fat, 25% protein, 5% carbs), and the main goal is to get the body into a metabolic state of enhanced fat burning called ketosis.
So how does it work?
Well, this requires a bit of biochemistry knowledge and understanding, but I’ll try to keep it simple.
Typically, our bodies use three different sources of fuel for energy: carbohydrates, proteins and fats. These so-called macromolecules are broken down, or metabolized, in different ways to provide fuel for our cells.
Carbohydrates are long chains of sugar molecules, and as we eat and digest a carbohydrate rich meal (and I DO love my pasta!), the chain of sugar molecules is broken down into its basic molecular building blocks - glucose. This causes a rise in the levels of blood glucose, which signals to particular cells in our pancreas to make insulin - a hormone that acts like a key to unlock our cells and allows glucose to travel out of our bloodstream. Once inside our cells, glucose is further broken down by a process known as glycolysis.
Any glucose that isn’t used up in our general day-to-day “energy expenditure” is then stored for use later on...if we need it. However, because we’re so well fed these days, this rarely happens, so instead it’s turned into fat through a process called lipogenesis.
In a similar way, fats are also long chain molecules, but when we break down fat to fuel our energy needs, it occurs through a process called beta oxidation - which basically just means the chain is “broken” at the second carbon along, which then gets an oxygen molecule attached to it and results in the production of a metabolite called acetyl CoA.
Under normal conditions, this product is further oxidized in a specialized structure inside the cell called the mitochondria, which is like a little factory that cranks out sugars and fats for our cells to use for energy. However, if there aren’t enough free carbohydrates available, or there’s too much acetyl CoA and the mitochondria can’t keep up, then this acetyl CoA is used to make ketone bodies - a useful source of energy for the brain, which actually receives 60-70% of its energy from ketones when blood glucose is low.
In fact, ketones are a more efficient fuel source than carbohydrates, and provide health benefits beyond weight loss, including:
But my burning question is this: how does the ketogenic diet prevent cancer?
Well, the answer lies (partly) in the inability of certain cancer cells to use ketones as a fuel source. The guiding principle here is that if a patient restricts their carbohydrate intake and therefore triggers ketosis, then the cancerous cells will effectively starve because of their inability to obtain energy from ketones.
Where’s the evidence?
Some studies using various different cell lines cultured in the lab, including glial and neural cell lines from the brain and nervous system, and liver cancer cell lines, have shown that cancer cells are unable to use ketone bodies as an energy source. Some of these cancer cell lines also lack the right enzymes needed to break down ketone bodies for energy.
Yet, still other studies show that even though certain cancer cells, such as in breast and prostate cancer, express these enzymes and can use ketone bodies for energy, the induction of ketosis by restricting calorie intake can reduce the rate of tumor growth and progression.
The most recent evidence, however, comes from a first-of-its-kind randomized controlled trial (the gold standard type of study in any medical intervention) in women with ovarian and endometrial cancer, which showed that the ketogenic diet reduced the amount of visceral fat (“deep belly fat”) without reducing their lean muscle mass, and also lowered their levels of insulin in the blood.
This trial also revealed lower levels of fasting insulin in patients following the ketogenic diet, suggesting improved insulin sensitivity, which in turn may be linked to the reduction of visceral fat, although the molecular mechanisms underlying this association isn’t clear.
Interestingly, this trial also found that as levels of a particular type of ketone body increased, the levels of a growth hormone called insulin-like growth factor 1 (IGF-1), which is known to stimulate cancer cell growth, decreased in the ketogenic patients. This so-called “inverse relationship” suggests that the ketogenic diet can produce an environment that actually limits cancer growth.
The bottom line
Overall, whilst the evidence is still only classed as “emerging” - i.e. scientists aren’t calling it “strong evidence” (yet), this “emerging evidence” is quite compelling for the role of the ketogenic diet as an adjunct therapy in preventing tumor growth and even initiation.
However, something quite obvious appears to be at play here: the ketogenic diet in these studies is resulting in weight loss in the patients who are participating. And it is well known that obesity is a major contributing factor to cancer risk and progression in the current climate. Therefore, it may simply be the case that reducing the amount of visceral fat is enough to reduce cancer risk and stunt its growth. And as we’ll see in the next of this series, fasting can bring many of the same physiological benefits.
A final word of caution, though: there are some concerns around the increasing number of anecdotal tales of clinicians recommending keto, or patients deciding to try it out for themselves, without the right assessment, individualization, education, monitoring and ongoing support.
All this to say, if keto isn’t for you (and it isn’t for everyone - it can be quite tricky to adhere to!), then perhaps try something else.
One more thing!
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