Why It’s Hard for Children with
Autism to Make Eye Contact

Many children with autism struggle to make eye contact with strangers, friends, and family.

One of the main criteria used to test for autism is full or partial eye contact (or lack thereof), with a preference for lateral, unfocused vision.

In the case of autism, partial eye contact may appear differently and with varying intensity. However, most children on the spectrum have real challenges making full or partial eye contact.

Some children only struggle to make partial eye contact in the presence of strangers. Others, however, experience the same challenges at home.

Similarly, some children on the autism spectrum have trouble pointing at objects they are interested in. Behavioral therapies tend to cite this behavior as a lack of social reciprocity and an overarching difficulty in developing emotional connections.

In addition to sensory overload causing children on the spectrum to struggle to make eye contact, there is a biochemical reason for this phenomenon. A lack of eye contact, or interrupted eye contact, among children with autism, is often a sign of a G protein disorder.

G protein controls the cellular signal and is critical to retinoid receptor function, forming the basis for healthy visual processing.

Lack of Eye Contact and the Cellular Signal

The cellular signal refers to the cells’ ability to perceive and respond correctly to their microenvironment. A lack-of-eye-contact disorder, combined with a vitamin A deficiency, may cause immune dysregulation, a weak immune response, or a low metabolism of lipids that are necessary for brain development.

Vitamin A deficiency or malabsorption causes destruction in the visual processing center of the brain, which can cause serious issues where visual planning manipulation is concerned.

However, the administration of vitamin A as a nutritional supplement may help to reconnect the retinoid receptors that are vital to vision, sensory perception, lingual processing, and attention.

This means that the first step in treating lack of eye contact in children with autism is the use of vitamin A in its natural form, with the aim of repairing the G protein and restoring good visual processing.

What Causes Vitamin A Deficiency?

There are a number of conditions that may cause vitamin A deficiency. These include:

1. Low protein and fat intake due to food fussiness.
2. Digestive disorders such as digestive enzyme deficiency, deficiency in bile acid synthesis or secretion into the intestine, chronic diarrhea, celiac disease, and inflammatory bowel disease (characteristic of some children on the autism spectrum).
3. Zinc deficiency which causes a decrease in enzyme activity that releases retinal from its stored form.
4. Zinc mineral deficiency, affecting the enzyme that oxidizes retinol into retinal.
5. Iron deficiency, which may cause vitamin A metabolism disorders and exacerbate iron deficiency (anemia).
6. Pancreatic disorders, or pancreatic dysfunction, causing improper secretion of the digestive enzymes necessary for vitamin A lysis and the absorption process.

 A serum blood test can identify vitamin A deficiency. Serum retinol levels of less than ten micrograms per deciliter indicate acute vitamin deficiency and the depletion of vitamin A reserves in the liver.

Eye Contact, Autism, and Vitamin A Reserve Replenishment Through Nutrition

There are two main ways to acquire vitamin A: from animals and from plant sources.

• Vitamin A replenishment from plants

Vitamin A is found in fruit and vegetables of the beta carotene family, which are converted into retinol (the alcohol form of vitamin A) after absorption.

These foods include cooked sweet potato, cooked butternut squash, cooked spinach, mustard leaves, carrots, parsley, dill, pumpkin, purple lettuce, cilantro, basil, chives, melon, and red peppers.

• Vitamin A replenishment from animals

Vitamin A is found in fish oil, beef liver, chicken liver, fatty cheese, and butter. Beta carotene is absorbed less easily in the intestine than retinyl palmitate, which is a precursor to retinol found in animal products like liver, egg protein, fish oil, milk, and butter.

This means that fruits and vegetables are ultimately less effective as a source of vitamin A.

Overall, great care must be taken when addressing a vitamin A deficiency with nutritional supplementation. Supplements should only be administered in an educated, controlled manner—under the guidance of a qualified therapist, and for a limited time only.

Excessive vitamin A uptake will result in toxicity and the rapid absorption of the vitamin in the intestine, peaking two to six hours after digestion. In contrast, the vitamin’s clearance from the body is slow.

Vitamin A toxicity may manifest as nausea, emesis, irritability, appetite loss, blurred vision, headaches, alopecia, abdominal pain, weakness, insomnia, dry mucosae, fever, anemia, or blurred consciousness. It may also result in loss of bone mass.

In most studies, however, lack of eye contact—or interrupted eye contact—in children on the spectrum may be treated with educated, short-term vitamin A supplementation.

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The information in this article is exclusively for general knowledge purposes. It should not be used for personal treatment or as a substitute for medical advice. There is no representation or warranty, explicit or implied, involving the accuracy, validity, or completeness of the content in this piece. Nutritional supplementation should only occur under the supervision of a licensed professional (and in accordance with laboratory test results).