Hippocrates is attributed with the concept of food as medicine. “Let thy food be thy medicine, and thy medicine be thy food.” But in today’s society, can food be medicine?
Many traditional medical physicians are quick to judge other clinicians who claim that food can “improve the symptoms of mental health disorders,” or when clinicians say that a good diet can “reverse” or even “cure” disease.
Let’s take a look at some of the literature to see what the “evidence” tells us.
Does food/glycemia/nutrition affect mood, including depression or anxiety?
There are quite a number of studies implicating various nutritional disorders with mental disease, namely B-12 deficiency, diabetes, and high-glycemic diets.
What about Food Quality and Food Security?
It seems as if food quality and food security play an intimate role in anxiety and depression.
Is there any evidence that a well-constructed, ketogenic diet could be beneficial?
I can tell you that many of my patients have been able to taper their anxiolytics and antidepressants with weight loss and diet improvement. There does seem to be some early evidence that a well-constructed ketogenic diet can help.
Since the 1920s, very-low-carbohydrate ketogenic diets (VLCKD) have been used as a therapy for epilepsy and can reduce or eliminate the need for medication. In fact, a recent Cochrane review demonstrated a 30–40% reduction in seizures compared with controls, “comparable to modern antiepileptic drug” therapy.
Since the 1960s and 1970s, VLCKD has been promoted widely for obesity treatment and weight loss, and it has become more commonly known as the “Atkins Diet.”
Ketogenic diets are characterized by reducing carbohydrates (usually to less than 50 g/day) and a relative increase in the proportions of protein and fat.
Insulin activates the pathways, which store energy derived from carbohydrates, causing lipogenesis and fat storage, reducing circulating glucose. In a VLCKD, there is a scarcity of dietary carbohydrates, which results in a reduced insulin level, and a secondary reduction in lipogenesis and fat accumulation.
Ketone bodies (acetoacetate, β-hydroxybutyric acid and acetone) are primarily produced by the mitochondria in the liver in a process called ketogenesis when insulin is low, and the diet is very-low carbohydrate. Ketones are then used by cells as a source of energy through a pathway that leads to formation of acetyl CoA from β-hydroxybutyrate.
Ketosis is a normal physiological mechanism described by biochemist Hans Krebs, who referred to physiological ketosis to differentiate it from the pathological ketoacidosis seen in type 1 diabetes. In physiological ketosis (which occurs during very-low-calorie ketogenic diets), ketonemia reaches maximum levels of 7-8 mmol/l and with no change in pH, whereas in uncontrolled diabetic ketoacidosis, it can exceed 20 mmol/l with a concomitant lowering of blood pH.
In individuals with insulin resistance, there is an impaired ability of muscle cells to take up circulating glucose. A person with insulin resistance will divert a greater proportion of dietary carbohydrate to the liver, where much of it is converted to fat (that is, de novo lipogenesis), as opposed to being oxidized for energy in skeletal muscle.
There is strong evidence that the use of ketogenic diets in weight-loss therapy is effective. The majority of ad-libitum studies demonstrate that subjects who follow a low-carbohydrate diet lose more weight during the first 3–6 months compared with those who follow balanced diets. There appears to be improved weight loss due to the direct appetite-suppressant action of ketosis; the increased metabolic costs of gluconeogenesis and the thermic effect of proteins, approximately a 25% conversion cost; the higher satiety effect of proteins (feeling full longer); and a reduction in lipogenesis and increased lipolysis, due to reduced insulin.
Signaling activities of ketone bodies regulate gene expression, inflammation, and metabolism, by specific signaling pathways:
Satiety of different foods is the feeling of fullness that lasts for a period after a meal, through a complex interaction between the Enteric Nervous System and the Central Nervous System.
The food choices we make determine our satiety, our sense of fullness and satisfaction with a meal. The sensation of satiety drives our downstream consumption (how hungry and how soon we are likely to eat after a meal). Processed foods lacks long-term satiety. The enteric nervous system is the home to most of the body’s serotonin and communicates directly to the central nervous system through the vagus nerve. The gut and its interactions with the presented nutrients is the basis of our “gut feeling.”
Satiety reduces decision fatigue while cravings take advantage of decision fatigue.
When you’re hungry or sleep deprived, your brain is more responsive to pictures of high-calorie food. Hungry people buy more calories when they go grocery shopping. You’re more sensitive to sweet and salty tastes when you’re hungry. If you’re going somewhere like a bar or a party where you know there will be junk food, don’t go hungry. Satiate with protein first to reduce decision fatigue.
Sleep deprivation also enhances brain sensitivity to pictures of high-calorie foods and reduces brain activity in areas responsible for deliberate cognitive control of food intake. Sleep deprivation reduces impulse control, and teenagers under experimental conditions of sleep deprivation eat more refined carbs, especially desserts and sweets. If you know that you will be confronted by tempting food, having a brain reset nap may also reduce decision fatigue.
Is diet a cure for any of these disease?
It is only possibly a part of the cure, but a bad diet can certainly exacerbate symptoms.
Can a well-constructed diet erase trauma, abuse or neglect?
It’s not likely, but it may help your coping mechanisms. A nutrient dense diet seems to be associated with a decreased burden of mental health issues as well as alleviating symptoms of depression and anxiety. There is plenty of strong evidence of iron excess, copper excess, folate deficiency, and other nutritional disorders that are implicated in psychiatric and mental health.