Dietary Causes of Vertigo (BPPV)

Benign paroxysmal positional vertigo, or BPPV for short, is a debilitating condition that causes severe room-spinning dizziness with changes of head position. If you’ve heard of ‘crystals being loose in the ear’, this is BPPV. It is usually called ‘idiopathic BPPV’, which simply means we don’t know the cause. Head trauma can cause it, but for many patients that deal with this, they haven’t had any trauma. Some recent research has proposed that there is likely a dietary component of this condition in the form of changes in carbohydrate metabolism. 

First, a quick overview on the inner ear. You have 3 semicircular canals in your inner ear. They are full of two layers of fluids, the endolymph and perilymph. The endolymph contains more potassium ions, and the perilymph contains more sodium ions. This gradient differential creates a potential to conduct nerve impulses. One suggestion of a possible dietary cause is as simple as an electrolyte imbalance, particularly sodium, as it may interfere with the nerve impulse. 

At the base of the semicircular canals, there is an organ called the utricle which has otoconia (the crystals) and hair cells attached to it. In BPPV, the otoconia degenerate and make their way into the canals, causing severe room-spinning dizziness. Degeneration has been linked to a number of causes, including vitamin D deficiency (Talaat et al. 2016). 

There also has been studies that show a correlation between dysfunctions in carbohydrate metabolism and BPPV. It is well known that chronically high levels of insulin can affect the cardiovascular system and cause hypertension. The endolymphatic sac has a high level of insulin receptors (Bittar et al. 2004). So it would follow that any problems with insulin, such as diabetes, would have an effect on inner ear function. The research supports this idea and in a Brazilian study conducted in 2015 (Webster et al.), followed a group of 72 patients that had BPPV, and followed them for 4 years. They found that recurrence of BPPV with patients that had hyperinsulinemia to be 4.6 times greater than those without, and recurrence of patients with hyperglycemia to be 2.47 times greater than the general population. Also, hyperinsulinemia has been associated with endolymphatic hydrops (a different form of dizziness) and there have been studies that have suggested endolymphatic hydrops may cause BPPV (Tanimoto et al., 2008). So perhaps hyperinsulinemia may be a common underlying cause.

Lastly, pH levels also appear to have an influence on the crystals. An acidic diet can cause erosion of the crystals. During sleep, shallow breathing can cause respiratory acidosis, and low blood pH. It is common for BPPV to happen first thing in the morning. Additionally, diabetes and gout can decrease blood pH, leading to BPPV (Han & Kim., 2020). 

Alas, more evidence that a high carbohydrate diet is probably not the best for everybody. The research is not conclusive, but there is a pretty strong signal.

Feeling Dizzy? We have a program that can help you resolve it, mostly on your own.

References: 

(PDF) vestibular impairment secondary to Glucose Metabolic ... (n.d.). Retrieved September 15, 2021, from https://www.researchgate.net/publication/262483036_Vestibular_impairment_secondary_to_glucose_metabolic_disorders_reality_or_myth. 

Han, D.-G., & Kim, D.-J. (2020). The evolutionary hypothesis of benign paroxysmal positional vertigo. Medical Hypotheses, 134, 109445. https://doi.org/10.1016/j.mehy.2019.109445 

Talaat, H. S., Kabel, A.-M. H., Khaliel, L. H., Abuhadied, G., El-Naga, H. A., & Talaat, A. S. (2016). Reduction of recurrence rate of benign paroxysmal positional vertigo by treatment of severe vitamin d deficiency. Auris Nasus Larynx, 43(3), 237–241. https://doi.org/10.1016/j.anl.2015.08.009 

Tanimoto H, Doi K, Nishikawa T, Nibu K. Risk factors for recurrence of benign paroxysmal positional vertigo. J Otolaryngol Head Neck Surg. 2008 Dec;37(6):832-5. PMID: 19128712.

Webster, G., Sens, P. M., Salmito, M. C., Cavalcante, J. D., dos Santos, P. R., da Silva, A. L., & de Souza, É. C. (2015). Hyperinsulinemia and HYPERGLYCEMIA: Risk factors for recurrence of benign paroxysmal positional vertigo. Brazilian Journal of Otorhinolaryngology, 81(4), 347–351. https://doi.org/10.1016/j.bjorl.2014.09.008 

Type 3 Diabetes

Type 3 diabetes is a new (and not quite accepted yet) term to describe the effects that diabetes can have on the brain. It describes the progression of diabetes to Alzheimer’s disease. The correlation between diabetes and Alzheimer’s is well documented, and this blog will aim to describe the proposed mechanism.

Just a quick reminder; diabetes is directly affected by insulin. There is either not enough insulin (type 1), or too much production due to insulin resistance (type 2). Type 2 diabetes is the one that is implicated in Alzheimer’s disease. 

Alzheimer’s is complicated, and the current understanding of the disease process postulates that progression is due to a build up of a protein called amyloid beta peptide. These form plaques that affect brain function. Your brain cells have receptors of insulin, so when it is released from the pancreas, it has a direct effect on the brain. When the brain becomes insulin resistant, more insulin has to be released to have the intended response. The plaques in patients with Alzheimer’s are formed in the space between nerves of the brain, not inside the nerves. An overabundance of insulin causes the nerves to release the amyloid beta protein into the space between the nerves (Gasparini et al., 2001). 

Alzheimer’s accounts for about 80% of all dementia. Vascular dementia is another form where the blood vessels aren’t functioning normally. There is a cause and effect relationship between hyperinsulinemia and hypertension. Insulin increases blood pressure by increasing sodium absorption in the kidneys, activating the fight or flight nervous system, and causing the blood vessels to thicken. Conversely, high blood pressure causes decreased delivery of insulin and glucose to the muscle cells, resulting in impaired glucose uptake (Salvetti et al., 1993). 

These are just a few of the mechanisms of how insulin resistance may be causing dementia. The more you read on insulin resistance, the more you learn just how horrible it is. For example, too much insulin will make you gain weight. Fat cells are like endocrine organs, meaning they can secrete signaling molecules. One of the molecules they secrete is cytokines, which cause inflammation. Inflammation causes further insulin resistance, which causes more inflammation, and the cycle repeats. This chronic systemic inflammation eventually reaches the brain. 

Another problem is that many people are insulin resistant and have not been diagnosed. If you are overweight and have high blood pressure, you are very likely to have insulin resistance. A few other signs of insulin resistance are dark patches of skin around the armpits and neck, and also skin tags which are little growths of skin. By the way, you don’t have to be overweight to be insulin resistant. You can be T.O.F.I., which stands for “thin on the outside, fat on the inside”. Fat can form around your organs. 

If you have some of these symptoms, you may want to speak to your physician about adopting a low carb, high fat diet. Also, you can order a self test kit to check your A1C. Find the test here, and use the code DPT20 for 20% off. 

References: 

Gasparini, L., Gouras, G. K., Wang, R., Gross, R. S., Beal, M. F., Greengard, P., & Xu, H. (2001). Stimulation of β-Amyloid Precursor Protein Trafficking by Insulin Reduces Intraneuronal β-Amyloid and Requires Mitogen-Activated Protein Kinase Signaling. The Journal of Neuroscience, 21(8), 2561–2570. https://doi.org/10.1523/jneurosci.21-08-02561.2001 

Salvetti, A., Brogi, G., Di Legge, V., & Bernini, G. P. (1993). The Inter-Relationship between Insulin Resistance and Hypertension. Drugs, 46(Supplement 2), 149–159. https://doi.org/10.2165/00003495-199300462-00024 

Why People with Hypoglycemia Should Eat a Low Carb Diet

Whatever it is, the way you tell your story online can make all the difference.

As a child, I was diagnosed with hypoglycemia. I had the typical symptoms; I was tired, shaky, irritable, and would have brain fog. My parents were told to keep me away from sweets and for years, I didn’t have candy. I remember even having pancakes with syrup would cause severe nausea and I’d have to lay down. I never really understood that if I had low blood sugar (hypoglycemia), why would putting sugar in the system bother me? It would seem that would be the way to fix it.

As usual, the answer to this is much more nuanced as it is the human body. It’s not just a simple input/output machine. Part of the answer is due to homeostasis, and the other part has to do with the endocrine system. 

I’ll give an analogy for the way homeostasis works. Imagine driving on a highway on a cold night, and you hit a patch of black ice. You start to fishtail out of control and then overcorrect the steering wheel to now fishtail in the opposite direction, but to a lesser extent. You tug the wheel back and forth until you finally straighten back out. This is how our bodies react to rapid swings in blood chemistry. 

When you eat a meal high in carbs, the endocrine system reacts by overcorrecting, for individuals that are carb sensitive. Insulin is secreted by the pancreas and wipes out the sugar by ushering it into muscle cells and the liver. Now the body is in a hypoglycemic state. 

The traditional medical answer is usually to add more sugar back into the system, but that is addressing the symptom rather than the root cause. Why not just stop eating high carb meals? The carbs are causing the spike in insulin and subsequent drop in blood sugar. Carbs are non-essential to the human diet. We are able to produce glucose in our bodies via the liver in a process called gluconeogenesis. 

One of the issues that arises in type 2 diabetics is insulin resistance. All cells have receptors for insulin, and when someone has a diet of high carbs over long periods of time, the receptors for insulin become resistant, and the cells don’t allow glucose in. Insulin has many functions, one of which is to suppress gluconeogenesis. So when the liver becomes insulin resistant, gluconeogenesis is not suppressed (Hatting et al., 2017). So now the liver is producing glucose, and more glucose is flooding the body through the diet. Now we are in a hyperglycemic state, and this is where much of the damage of sugars occur, furthering the disease process of diabetes. 

Glucagon is another player in this situation. It has the opposite effect of insulin; it draws sugars out of cells back into the bloodstream. Why not increase glucagon in the diet when we are in a hypoglycemic state? Turns out that eating a moderate amount of protein can stimulate glucagon secretion (Schmid et al., 1989). 

In short, a diet low in carbs and high in proteins and fats will keep blood sugars at normoglycemic levels, and can prevent the development of metabolic dysfunction. 

References:

Hatting, M., Tavares, C. D., Sharabi, K., Rines, A. K., & Puigserver, P. (2017). Insulin regulation of gluconeogenesis. Annals of the New York Academy of Sciences, 1411(1), 21-35. doi:10.1111/nyas.13435

Schmid, R., Schusdziarra, V., Schulte-Frohlinde, E., Maier, V., & Classen, M. (1989). Role of amino acids in stimulation of POSTPRANDIAL INSULIN, Glucagon, and Pancreatic POLYPEPTIDE in humans. Pancreas, 4(3), 305-314. doi:10.1097/00006676-198906000-00006