Hypotonia and Nutrition

Low muscle tone, or hypotonia, is one of the physical problems often associated with developmental delays; nutrition and low muscle tone are intimately connected. Children can have generalized hypotonia or it may affect just specific areas such as the hands or upper body.

Hypotonia is clinically significant because in severe cases the muscles are literally too weak to perform important tasks such as holding a pencil or sitting without slumping in a chair. In milder cases, stamina or precision are affected.

For example, children with severe hypotonia of the hands are reluctant or sloppy writers whose interest in writing or drawing declines in direct correlation with the severity of the low tone. When the concerns are milder, youngsters may try to overcompensate for difficulties by holding pencils too hard and causing cramps or creating blisters.

Hyptonia Causes

There are two possible causes of hypotonia: vestibular issues and nutritional deficiencies (or both).

Vestibular Issues

Occupational therapists contend that vestibular system imbalances are to blame for low muscle tone. The vestibular system is the primitive sensory system that is responsible for gravitational stability. The ability to walk down a flight of stairs while carrying a load of laundry is a tribute to the gravitational stability provided by a well-functioning vestibular system.

People described as clumsy or children with difficulty climbing or riding bicycles often have vestibular issues. Good muscle development (or how your body pushes against gravity) is also considered a marker of vestibular development.

Nutritional Deficiencies

From a nutritional perspective, hypotonia represents the poor delivery of nutrients to the muscles. Diet represents what is consumed, but nutrition is what the tissues actually get.

When soft muscles are present, there is a big gap between diet and nutrition. The muscles, suffering from nutrient deprivation, remain underdeveloped, or if strong, become fatigued easily.

Congenital hypotonia is not the same as being out of shape. Those born with low tone can improve their condition but the tendency will remain. That is, if two people exercise exactly the same amount, the one with hypotonia will have less muscle development as a result.


If the delivery of nutrients is inefficient, there are two basic strategies to better manage the situation: increase the amount of nutrients available for transport and try to regulate the naturally sluggish dispatch system.

Those with hypotonia tend to love sweets as they are a quick form of energy for tired muscles, but in the long run, a diet high in empty calories worsens the deficit. Controlling the intake of concentrated sugars (candies, sodas, juice, desserts) is the first step followed by the usage of a comprehensive multiple vitamins and minerals.

Because even a perfect diet will not be enough for someone with poor nutrient distribution, extra nutrients will assure that minimum requirements are met. However, the use of supplemental nutrients is a long term management tactic, not a quick fix.

Once there are plenty of general nutrients to deliver, one can attempt to strengthen assimilation and usage of nutrients with more sophisticated measures. Digestive enzymes, carnitine, and co-enzyme Q-10 all may help. For specific information on supplements for your child, always confer with a health care professional.

Digestive Enzymes

Digestive enzymes aid the breakdown and assimilation of food. If used too aggressively, they cause stomach cramps and loose stools. They are given with meals, preferably lunch and dinner, as the body’s strongest capacity for digestion is in the morning and so they are less needed then.

Vegetable-based enzymes, such as Prevail Children’s Digestion, are gentlest.

In addition to low tone, those who do best with enzymes tend to be picky eaters, have digestive complaints such as stomach aches and/or have constipation or diarrhea.


Carnitine (or L-carnitine, the active form) is critical for regulating fat burning (i.e., energy availability) in muscles. L-carnitine is made by the liver from the amino acids methionine and lysine with the help of vitamins C, B-6 and niacin.

Dietary sources are muscle and organ meats. There is no carnitine in vegetables, fruit, or grains.

In diseases with muscle deterioration, carnitine almost always helps and low carnitine is often a marker. Those with low tone may likewise benefit from carnitine even though their situation is not as profound. L-carnitine is non-toxic, and 500-1,000mg is a typical dose range.


The body cannot use food directly for energy but must convert it to an energy holding compound called ATP. There is only enough ATP stored in the body to provide energy for about five to eight seconds of non-stop strenuous activity, so it must be constantly re-generated using co-enzyme Q-I0 (or ubiquinone). Co-enzyme Q-10 nutritional supplementation would, therefore, be important for muscle performance and stamina.

One preliminary study found co-enzyme Q-10 improved muscle work capacity in normal volunteers. Studies also show that co-enzyme Q-10 appears to improve immune function. See Sources & References below for information on these studies.

The beginning dose range for co-enzyme Q-10 (like L-carnitine, a nontoxic substance) is usually 30-60 mg. L-carnitine and co-enzyme Q-10 can be taken safely together with a multi-vitamin to aid in their utilization.

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Sources & References

Dehley, Leanna M., et al. The Effect of Mitochondrial Supplements on Mitochondrial Activity in Children with Autism Spectrum Disorder. J Clin Med. 2017 Feb; 6(2): 18.

Filipek, P.A., et al. Relative carnitine deficiency in autism. J Autism Dev Disord. 2004 Dec;34(6):615-23.

Hao, J., et al. Mitochondrial nutrients improve immune dysfunction in the type 2 diabetic Goto-Kakizaki rats. J Cell Mol Med. 2009 Apr;13(4):701-11.

Liu, J. The effects and mechanisms of mitochondrial nutrient alpha-lipoic acid on improving age-associated mitochondrial and cognitive dysfunction: an overview. Neurochem Res. 2008 Jan;33(1):194-203.

Long, J., et al. Mitochondrial decay in the of old rats: ameliorating effect of alpha-lipoic acid and acetyl-L-carnitine. Neurochem Res. 2009 Apr;34(4):755-63.

Mabalirajan, U., et al. Effects of vitamin E on mitochondrial and asthma features in an experimental allergic murine model. J Appl Physiol. 2009 Oct;107(4):1285-92.

Maes, M., et al. Coenzyme Q10 deficiency in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardiovascular disorder. Neuro Endocrinol Lett. 2009;30(4):470-6.

Maes, M., et al. Lower plasma Coenzyme Q10 in depression: a marker for treatment resistance and chronic fatigue in depression and a risk factor to cardiovascular disorder in that illness. Neuro Endocrinol Lett. 2009;30(4):462-9.

Noland, R.C., et al. Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control. J Biol Chem. 2009 Aug 21;284(34):22840-52.

Power, R.A., et al. Carnitine revisited: potential use as adjunctive treatment in diabetes. Diabetologia. 2007 Apr;50(4):824-32.

Shen, W., et al. Protective effects of R-alpha-lipoic acid and acetyl-L-carnitine in MIN6 and isolated rat islet cells chronically exposed to oleic acid. J Cell Biochem. 2008 Jul 1;104(4):1232-43.

Shekhawat, P.S., et al. Spontaneous development of intestinal and colonic atrophy and inflammation in the carnitine-deficient jvs (OCTN2(-/-)) mice. Mol Genet Metab. 2007 Dec;92(4):315-24.

Spindler, M., et al. Coenzyme Q10 effects in neurodegenerative disease. Neuropsychiatr Dis Treat. 2009;5:597-610.

Zhang, H., et al. Combined Ralpha-lipoic acid and acetyl-L-carnitine exerts efficient preventative effects in a cellular model of Parkinson’s disease. J Cell Mol Med. 2010 Jan;14(1-2):215-25.