Essential fatty acids (EFAs) are fats the human body cannot manufacture, meaning they must be obtained entirely through diet. This need defines them as “essential” nutrients for survival and proper bodily function. While true Essential Fatty Acid Deficiency (EFAD) is uncommon in the general population, it is a serious nutritional problem when it occurs, potentially leading to significant health complications. Understanding the signs of this deficiency is important for individuals with risk factors, as early detection can prevent long-term health issues.
Identifying Essential Fatty Acids and Their Roles
Essential fatty acids are polyunsaturated fats categorized into two main families: Omega-3 and Omega-6. The two specific EFAs the body requires are Linoleic Acid (LA), an Omega-6, and Alpha-Linolenic Acid (ALA), an Omega-3. Dietary intake is mandatory because the body lacks the specific enzymes needed to synthesize them.
These fatty acids are incorporated directly into the structure of cell membranes, influencing fluidity and the function of embedded proteins. They are also precursors to signaling molecules called eicosanoids, which regulate processes like inflammation, blood clotting, and blood pressure. Omega-3 fatty acids, such as DHA and EPA derived from ALA, are important components of the retina and the brain’s neuronal cell membranes. A regular supply of these fats is necessary to maintain cellular integrity and support the nervous system.
Causes and Populations Most at Risk
EFAD arises when the body fails to receive or adequately absorb sufficient quantities of LA and ALA. It rarely results from a simple poor diet in a healthy person, but rather occurs in specific clinical settings.
Clinical Causes
One primary cause is the prolonged use of parenteral nutrition (IV feeding) that lacks adequate lipid injectable emulsions (ILE). While fats are routinely included now, shortages of ILE products or conditions requiring restricted IV fat intake, such as severe hypertriglyceridemia, still place patients at risk.
Malabsorption and Surgery
Malabsorption disorders significantly increase the risk of EFAD because they impair the body’s ability to extract fats from food. Conditions like cystic fibrosis, chronic pancreatitis, and exocrine pancreatic insufficiency reduce the availability of enzymes needed for fat digestion. Patients who have undergone specific gastrointestinal surgeries, such as bariatric procedures or massive bowel resection, may also experience reduced absorption capacity.
Vulnerable Populations
Infants and children are particularly vulnerable, especially premature neonates who lack sufficient adipose stores. Low-fat or non-fortified infant formulas can quickly lead to deficiency in this population. Adults who are severely malnourished or follow extremely fat-restricted diets for extended periods, such as those with a chyle leak, deplete their existing fat stores and are also at heightened risk.
Recognizing the Physical Signs of Deficiency
The most visible and common signs of EFAD often manifest on the skin, reflecting the fatty acids’ role in maintaining the skin barrier. A generalized, dry, and scaly dermatitis, sometimes resembling eczema or ichthyosis, is a hallmark symptom. This condition, known as desquamating dermatitis, can lead to increased water loss from the skin.
Another characteristic dermatological sign is follicular keratosis, which presents as raised, dry bumps around the hair follicles. The deficiency can also affect the health of hair and nails, causing hair loss (alopecia), dull or dry hair, and soft or brittle nails. Beyond the skin, EFAD results in poor or slow wound healing.
In infants, failure to thrive or decreased growth is a significant physical sign. Neurological symptoms can also occur, including visual impairment and subtle signs of peripheral neuropathy, given the importance of Omega-3 derivatives like DHA in the nervous system. The biochemical indicator of EFAD is an elevated triene:tetraene ratio, where the body produces Mead acid (a triene) in place of Arachidonic acid (a tetraene).
Treatment and Dietary Correction
The initial step in correcting EFAD is to restore adequate intake of LA and ALA. For severe, clinically complicated cases, treatment often involves the administration of intravenous lipid emulsions (ILE) in hospitalized patients. Increasing the ILE dosage corrects both the biochemical markers and the visible physical manifestations of the deficiency.
For patients who can tolerate oral or tube feeding, dietary management is the preferred course. This involves providing sufficient essential fatty acids through food or specialized formulas.
Dietary Sources
To obtain the necessary EFAs, sources include:
- Linoleic Acid (Omega-6): Vegetable oils like soybean, corn, and safflower oil.
- Alpha-Linolenic Acid (Omega-3): Flaxseeds, walnuts, and chia seeds.
Consuming fatty fish, like salmon and mackerel, provides the longer-chain Omega-3s, EPA and DHA, directly. Supplements, such as fish oil or flaxseed oil, can also be utilized. Consultation with a healthcare provider is important for diagnosis and to determine the necessary personalized treatment plan, as the required dose depends on the individual’s underlying condition.