Mitochondrial Dysfunction: The Role of Nutritional Supplementation

Mitochondrial Dysfunction: The Role of Nutritional Supplementation

Mitochondrial health

mitochondrial dysfunction and nutrition

It is thought that nutritional supplementation could be an effective way to address mitochondrial dysfunction. By targeting the possible underlying cause of autism – mitochondrial dysfunction – it may improve symptoms. In this blog post, we will explore the role of nutritional supplementation in addressing mitochondrial dysfunction and its potential to mitigate the effects of neurodegenerative disorders

What is mitochondrial dysfunction?

Mitochondrial dysfunction is a condition in which the mitochondria, the cells’ powerhouses, do not function properly. Mitochondria produce energy for the cell to use, and when they are not working correctly, it can lead to a variety of health issues, including neurological disorders such as Alzheimer’s, Parkinson’s, and ALS (Amyotrophic Lateral Sclerosis).
The mitochondria are responsible for producing energy in the form of adenosine triphosphate (ATP). ATP is necessary for a variety of cellular activities and processes, including muscle contraction, neural transmission, and DNA replication. Mitochondrial dysfunction can lead to a decrease in ATP production and result in a range of symptoms and complications. Symptoms may include fatigue, muscle weakness, difficulty thinking, brain fog, depression, and anxiety.
In neurodegenerative disorders such as Alzheimer’s, Parkinson’s, and ALS, mitochondrial dysfunction is believed to play an important role in the progression of the disease. Recent studies have suggested that impaired mitochondrial function contributes to the development of neurodegenerative disorders by leading to the accumulation of toxic proteins in neurons that contribute to neurodegeneration. Additionally, mitochondrial dysfunction may cause an increase in oxidative stress, which can damage neurons and lead to neurodegeneration.

How are mitochondrial dysfunction and autism linked?

Mitochondrial dysfunction has been strongly linked to autism spectrum disorders (ASD).

Research indicates that impaired mitochondrial function can disrupt the development of neural networks that are essential for cognitive and behavioral regulation—core domains affected in ASD. Since mitochondria are responsible for producing cellular energy (ATP), reduced mitochondrial activity can impair cell signaling and overall cellular function. This disruption can interfere with communication between different regions of the brain, which is believed to contribute to ASD-related symptoms.

In addition to these functional effects, mitochondrial dysfunction has been associated with genetic mutations frequently observed in individuals with autism-related conditions. These mutations may play a role in both the physiological and behavioral characteristics of ASD.

Furthermore, studies have shown that mitochondrial dysfunction often results in elevated oxidative stress. Oxidative stress can damage neuronal cells and disrupt synaptic communication, contributing to cognitive deficits, memory impairments, and learning difficulties frequently observed in ASD.

Overall, mitochondrial dysfunction is increasingly recognized as a significant factor in the pathophysiology of autism.
A deeper understanding of this connection could pave the way for more targeted interventions aimed at improving neurodevelopmental outcomes in individuals with ASD.

Can nutritional supplementation help?

Nutritional supplementation has long been recognized as a valuable tool for enhancing overall health, particularly in the context of neurological disorders.
Research has shown that specific nutrients may play a beneficial role in the management of neurodegenerative conditions, including those linked to mitochondrial dysfunction.

Several studies have highlighted the importance of vitamins and minerals, such as vitamin B12, in mitigating the effects of mitochondrial impairment. Vitamin B12 is essential for cellular energy production and helps prevent oxidative stress—a key factor associated with mitochondrial dysfunction. Other critical nutrients include thiamine (vitamin B1), magnesium, and omega-3 fatty acids, all of which support mitochondrial integrity and function.

Additionally, antioxidants play a crucial role in protecting cells from oxidative damage. Compounds like glutathione and coenzyme Q10 (CoQ10) help neutralize free radicals and reduce the oxidative stress that can damage mitochondrial structures. These antioxidants also support the repair and regeneration of compromised cells.

Beyond supplementation, dietary interventions can be highly effective in supporting mitochondrial health. A nutrient-rich diet—featuring an abundance of fruits, vegetables, whole grains, lean proteins, and healthy fats—can enhance cellular energy levels and provide the essential cofactors needed for optimal mitochondrial function.

In summary, nutritional strategies—ranging from targeted supplements to well-balanced dietary patterns—can help manage symptoms associated with mitochondrial dysfunction and neurodegenerative disorders.
However, it is important to consult with a healthcare provider before starting any new supplement regimen, as some nutrients may interact with medications or cause adverse effects at high doses.

Nutritional Supplements Supporting Mitochondrial Health

Nutritional supplementation can be a strategic approach to support mitochondrial function and mitigate the effects of mitochondrial dysfunction. The following supplements have been identified for their potential benefits:

  • Vitamin B12 (Methylcobalamin): Essential for energy production and reducing oxidative stress, vitamin B12 supports mitochondrial function and overall neurological health.

  • Coenzyme Q10 (Ubiquinone): A critical component of the electron transport chain, CoQ10 facilitates ATP production and acts as a potent antioxidant, protecting mitochondria from oxidative damage.

  • L-Carnitine: This amino acid derivative transports long-chain fatty acids into mitochondria for beta-oxidation, enhancing energy production and reducing fatigue.

  • Alpha-Lipoic Acid (ALA): A powerful antioxidant that regenerates other antioxidants and supports mitochondrial energy metabolism.

  • N-Acetylcysteine (NAC): Precursor to glutathione, NAC replenishes intracellular glutathione levels, aiding in detoxification and reducing oxidative stress.

  • Pyrroloquinoline Quinone (PQQ): A redox cofactor and antioxidant, PQQ stimulates mitochondrial biogenesis, enhances mitochondrial function, and protects against oxidative stress. Studies suggest that PQQ supplementation may improve cognitive function, reduce inflammation, and support cardiovascular health.

  • Creatine: Supports rapid ATP regeneration, particularly beneficial in tissues with high energy demands like the brain and muscles.

  • Magnesium: A cofactor in over 300 enzymatic reactions, magnesium is vital for ATP synthesis and maintaining mitochondrial membrane potential.

  • Resveratrol: Activates sirtuins and PGC-1α, promoting mitochondrial biogenesis and improving metabolic function.

  • Curcumin: Exhibits antioxidant and anti-inflammatory properties, protecting mitochondria from oxidative damage and supporting overall cellular health.

Conclusion

Addressing mitochondrial dysfunction through targeted nutritional supplementation offers a promising avenue for improving symptoms associated with neurodegenerative diseases and ASD. Incorporating these supplements, under the guidance of a healthcare professional, can support mitochondrial health and enhance overall well-being.

Resources

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9604531/

The Relationship Between Autism and Mitochondrial Dysfunction

The Relationship Between Autism and Mitochondrial Dysfunction

Mitochondrial health

Relation between mitochondrial dysfunction and asd

Recent studies have revealed a potential connection between autism and mitochondrial dysfunction.
A systematic review and meta-analysis conducted by D.A. Rossignol and R.E. Frye provide compelling evidence of an association between autism spectrum disorders (ASD) and mitochondrial abnormalities. This finding has significant implications for understanding both the underlying mechanisms and possible therapeutic approaches for autism.

In this blog post, we will delve into the relationship between autism and mitochondrial dysfunction and explore what this connection could mean for individuals on the spectrum and the broader autism community.

Mitochondria are often referred to as the “powerhouses” of the cell because they generate adenosine triphosphate (ATP), the primary energy currency of the cell. They achieve this through a process called cellular respiration, converting nutrients from food into usable energy. Beyond energy production, mitochondria are involved in other critical functions, including regulating cell death (apoptosis), calcium storage, and the generation of reactive oxygen species (ROS).​

What Are Mitochondrial Disorders?

Mitochondrial disorders arise when the mitochondria fail to function correctly, leading to insufficient energy production. These disorders can be caused by mutations in mitochondrial DNA (mtDNA) or nuclear DNA that affect mitochondrial function. The impact of mitochondrial dysfunction can vary widely, depending on which cells and organs are affected.​

Common Symptoms

Symptoms of mitochondrial disorders can range from mild to severe and may include:​

  • Muscle weakness or pain​

  • Neurological problems (e.g., seizures, developmental delays)​

  • Gastrointestinal issues​

  • Cardiac problems​

  • Vision and hearing loss​

  • Respiratory complications​

  • Fatigue​

The severity and combination of symptoms can differ significantly among individuals, even within the same family.

Mitochondrial Dysfunction and Autism

Emerging research suggests a link between mitochondrial dysfunction and autism spectrum disorders (ASD). Some studies have found that a subset of individuals with ASD exhibit signs of mitochondrial dysfunction, such as abnormalities in energy metabolism and increased oxidative stress. However, it’s important to note that mitochondrial dysfunction is just one of many factors that may contribute to the development of ASD, and not all individuals with ASD have mitochondrial issues.​

Potential Triggers and Risk Factors

While many mitochondrial disorders are genetic, certain environmental factors may exacerbate mitochondrial dysfunction or trigger symptoms in predisposed individuals. These factors can include:​

  • Infections​

  • Exposure to toxins​

  • Certain medications​

  • Prolonged stress​

It’s crucial to approach these factors with scientific rigor, as the interplay between genetics and environment in mitochondrial disorders is complex and not fully understood.​

Diagnosis and Management

Diagnosing mitochondrial disorders can be challenging due to the variability in symptoms. A comprehensive evaluation may include:​

  • Detailed medical history and physical examination​

  • Laboratory tests (e.g., blood and urine analyses)​

  • Imaging studies​

  • Muscle biopsies​

  • Genetic testing​

While there is currently no cure for mitochondrial disorders, management strategies focus on alleviating symptoms and improving quality of life. These may involve:​

  • Nutritional support​

  • Physical and occupational therapy​

  • Medications to manage specific symptoms​

  • Avoidance of known triggers

Method of the study

The study performed a systematic review and meta-analysis of published studies examining the association between mitochondrial dysfunction and autism spectrum disorder (ASD). The authors searched databases such as PubMed, Cochrane, and Embase for relevant studies that met their inclusion criteria. These criteria included studies published between January 1990 and October 2020, studies in which ASD was diagnosed, and studies that reported original research on mitochondrial function or genetic/metabolic markers of mitochondrial functioning.
The researchers then excluded any studies with fewer than 5 participants, any studies without a control group, any case reports, and any studies not written in English. A total of 23 studies with 1298 participants met all the inclusion criteria and were included in the meta-analysis. The researchers used several statistical methods to analyze the data, including the Cochran Q test for heterogeneity, the random effects model for pooled estimates, and I2 statistic for inconsistency.

Results

The systematic review and meta-analysis conducted by Rossignol and Frye analyzed 11 studies on mitochondrial dysfunction in Autism Spectrum Disorders (ASDs). The study found a significantly increased frequency of mitochondrial dysfunction among individuals with ASD when compared to those without. Specifically, the analysis showed that individuals with ASDs had a 5.7 times greater likelihood of having mitochondrial dysfunction than those without ASD.
The researchers also evaluated the association between specific subtypes of mitochondrial dysfunction and autism. They found that abnormalities in oxidative phosphorylation (OXPHOS) were most commonly associated with ASD. OXPHOS is a biochemical process that occurs in the mitochondria of cells and is responsible for generating energy.
The researchers further assessed the relationship between mitochondrial dysfunction and clinical characteristics of ASD such as age, gender, severity, and cognitive impairment. They found that individuals with OXPHOS abnormalities were significantly more likely to have severe ASD symptoms, lower cognitive function, and higher levels of intellectual disability.
Overall, the results of this systematic review and meta-analysis suggest a strong link between mitochondrial dysfunction and ASD. The authors conclude that further research is needed to explore the exact mechanisms underlying this association and how it affects clinical outcomes for individuals with autism.

Discussion

The results of this systematic review and meta-analysis suggest a clear relationship between mitochondrial dysfunction and autism spectrum disorders. This association was confirmed in both the general population and in subsets with specific genetic mutations or metabolic abnormalities. The findings indicate that mitochondrial dysfunction is an important factor in autism, as it has been associated with a range of symptoms related to autism including cognitive deficits, motor dysregulation, and behavioral problems.
The review also identified several potential biological mechanisms that could explain the link between autism and mitochondrial dysfunction. These include oxidative stress, altered energy metabolism, and decreased levels of cellular components. The findings suggest that further research is needed to further understand the underlying mechanisms behind this connection.
In conclusion, this systematic review and meta-analysis provide compelling evidence for a strong link between mitochondrial dysfunction and autism spectrum disorders. Future research should focus on elucidating the biological mechanisms behind this association to gain a better understanding of the role of mitochondrial dysfunction in autism.

Conclusion

This systematic review and meta-analysis of studies investigating mitochondrial dysfunction in autism spectrum disorders provide strong evidence that there is a relationship between the two. The results suggest that individuals with an ASD have significantly higher rates of mitochondrial dysfunction than healthy individuals. Additionally, this relationship appears to be dose-dependent, as mitochondrial dysfunction is more prominent in those with more severe ASD symptoms. While further research is needed to explore the causal relationship between mitochondrial dysfunction and ASD, this review provides compelling evidence of a connection that must be further investigated. Clinically, the findings could inform diagnostic approaches to help identify individuals at risk for mitochondrial dysfunction and potentially lead to the development of novel treatments for individuals with autism spectrum disorders.

Note: This article is for informational purposes only and is not a substitute for professional medical advice. Always consult with a qualified healthcare provider for diagnosis and treatment options.

Resources

Rossignol, D., Frye, R. Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis. Mol Psychiatry 17, 290–314 (2012). https://doi.org/10.1038/mp.2010.136

  •  
Mitochondrial disorders

Mitochondrial disorders

Mitochondrial health

mitochondrial disorder

While the exact causes of autism are still unknown, researchers have recently uncovered a mysterious link between autism and mitochondrial disorders. Mitochondrial disorders are caused by mutations in the mitochondria, which are the parts of our cells that produce energy, and can lead to a wide range of symptoms. This link has made it possible to identify and treat some cases of autism, offering hope to those affected by this condition. In this blog post, we’ll discuss the intriguing connection between autism and mitochondrial disorders and what this could mean for those living with autism.

Mitochondria

The human body requires energy in order to function, and mitochondria are what provide that energy. We digest sugar, protein, and fat into molecules that reach every cell in our body. ATP is the fuel that is used by the body, and mitochondria are little factories within cells that convert these food molecules into energy molecules called ATP. 
Mitochondria are also called the energy-producing powerhouses of the body. They are vital to our survival as they produce energy in the form of ATP (adenosine triphosphate) from the food we eat. This process is called cellular respiration. Mitochondria produce more than 90% of the energy needed by the body to sustain life and support organ function. Mitochondrial dysfunction results in excessive fatigue and other symptoms that are common in almost every chronic disease, from Alzheimer’s disease and cardiovascular disease to diabetes to autism.

Mitochondrial disorder

The mitochondrial disorder can strike both infants and children of all ages and yet is NOT KNOWN what causes the dysfunction in the mitochondria in the first place. They are commonly born with a range of difficulties from lack of muscle tone to lack of strength and poor appetite, difficulty sucking and high tolerance to pain.
Some babies might not show noticeable symptoms right away. For example, when the body is under a significant amount of stress, it requires even more energy. Though a child can get very sick if mitochondria are dysfunctional, there are times when you’ll see problems developing with the child’s neurology if there’s a prolonged illness.
Yes, vaccines are also stressful for the body, and in the case of a small child who, for some reason, has a genetic predisposition to the mitochondrial disorder, it is possible that the child’s development stops after vaccination
At least 50% of children living with autism has mitochondrial disfunction.

Mitochondrial disorders are a group of complex and potentially life-threatening illnesses caused by mutations in the mitochondrial DNA. Mitochondria are tiny organelles found inside our cells that play a key role in energy production. They convert energy from food into a form that our bodies can use to function normally.

When the mitochondrial DNA is mutated, the resulting disorder can affect any part of the body, including the heart, brain, muscles, or other organs. Symptoms can vary from person to person, but can include seizures, developmental delays, movement and coordination problems, muscle weakness, vision and hearing loss, and organ failure. In some cases, these disorders may be fatal.
The exact cause of mitochondrial disorders is unknown, but certain genetic factors can increase an individual’s risk. It is important to note that not all people with mitochondrial disorders will develop autism, but research has shown that there may be a link between the two conditions.
Abnormalities of mitochondrial function could affect about 80% of children with ASD. 

Sympoms of mitochondrial dysfunction

Depending on which cells in the body are affected by the malfunctioning of the mitochondria, it causes varying symptoms. In general, mitochondrial disease causes more severe symptoms when the cell makers in the muscles, brain, or nerves malfunction because these cells use more energy than other cells in the body. In general, symptoms can range from mild to severe, affect one or more organs, and appear at any age. Even people with the same mitochondrial disease may have different symptoms. In addition to both symptoms and severity, the onset of the disease (appearance of symptoms) also varies from person to person.

The most common symptoms are fatigue, but brain fog is also common when the mitochondria in the brain are not working properly.

Other symptoms may include:

  • pain
  • mood disorders
  • anxiety
  • depression
  • concentration disorder

Most chronic diseases/conditions are also linked to mitochondrial dysfunction, such as:

  • cardiovascular diseases
  • lung disease
  • vision and hearing problems
  • learning disabilities
  • autism
  • liver and kidney disease
  • digestive system diseases and symptoms
  • diabetes
  • neurological diseases (including dementia)
  • movement disorders

The Hannah Poling affair

During Hannah’s first 18 months, she suffered an adverse reaction to the 18-month-old vaccine, causing severe neurological and autistic symptoms. Hannah was 19 months when she received five vaccinations (diperte, influenza B, MMR, varicella, and inactivated polio). Hannah was a playful, interactive, and communicative baby two days prior to becoming lethargic, irritable, and feverish two days later. Several days after vaccination, he developed varicella-induced rashes.
 
Hannah was diagnosed with mitochondrial enzyme deficiency encephalopathy months later due to a delay in neurological and psychological development. The signs Hannah displayed all exhibited characteristics of autism spectrum disorder, including language and communication difficulties. It is common for children with mitochondrial enzyme deficiencies to develop neurological symptoms during the first and second years of their lives, but Hannah’s parents believed vaccines led to her disease.
His case in court was successful, though it’s unclear whether the little girl had a mitochondrial disorder prior to the vaccination, or if it was caused by a vaccination reaction.

If the child has a mitochondrial enzyme deficiency, the vaccines can cause developmental declines.

Biomedical specialists believe that mitochondrial problems can be very common in autism; however, there are treatments that can improve mitochondrial disorders.

It would be nice if mitochondrial testing could become part of normal neonatal screening to find out which babies may be more sensitive to heavy metals and chemicals — whether they have “only” mitochondrial dysfunction or mitochondria are functioning completely abnormally — and preventive measures could be taken to protect children.

If the child has a mitochondrial enzyme deficiency, the vaccines can cause developmental declines.

Biomedical specialists believe that mitochondrial problems can be very common in autism; however, there are treatments that can improve mitochondrial disorders.

It would be nice if mitochondrial testing could become part of normal neonatal screening to find out which babies may be more sensitive to heavy metals and chemicals — whether they have “only” mitochondrial dysfunction or mitochondria are functioning completely abnormally — and preventive measures could be taken to protect children.

Related articles:

  • Mitochondrial disorder and autism
  • Supplements for mitochondrial disorders
Resources
  • https://www.sciencedirect.com/science/article/pii/S2352304220300854
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5137782/

Omega 3 fatty acid

Omega 3 fatty acid

Autism and Genes, Health, Mitochondrial health

Omega-3 fatty acids belong to the group of polyunsaturated fatty acids, of which EPA (eicosapentaenoic acid), DHA (docosahexaenoic acid), and alpha-linolenic acid (ALA) are best known. Omega-3 has many properties that help maintain our health, and are an essential bioactive ingredient for children.

omega 3

Omega 3 is mainly an anti-inflammatory agent.

EPA has a strong anti-inflammatory effect and not enough DHA in the diet may reduce the ability to handle sensory input. It only takes a small decrement in brain DHA to produce losses in brain function. (1)

In humans, weak sensorimotor gating is a hallmark of many nervous-system disorders such as schizophrenia or ADHD. Given mounting evidence of the role omega-3s play in the nervous system, there is intense interest in their therapeutic potential, perhaps as a supplement to medicines. For example, people with schizophrenia have lower levels of essential fatty acids, possibly from a genetic variation that results in poor metabolism of these nutrients.

The finding connects low omega-3s to the information-processing problems found in people with schizophrenia; bipolar, obsessive-compulsive, and attention-deficit hyperactivity disorders; Huntington’s disease; and other afflictions of the nervous system.

Omega 3 fatty acid

Omega 3 fatty acid belongs to the group of polyunsaturated fatty acids, of which EPA (eicosapentaenoic acid), DHA (docosahexaenoic acid), and alpha linolenic acid (ALA) are best known. Omega 3 is an essential fatty acid.

Consumption of much marine fish is no longer recommended today due to the pollution of the seas. The most practical solution for consuming EPA, DHA, and GLA is by using high-quality fish oil, borage oil, or evening primrose oil in encapsulated form.

Main physiological effects of histamine intolerance and intestinal problems:

In terms of histamine intolerance, its main effect is its ability to reduce stress and reduce inflammation.

It also helps prevent the development of insulin resistance and has a positive effect on weight loss by helping to break down fat cells.

Physiological effects of Omega 3:

  • Due to their anti-inflammatory effect, it can reduce the risk of many diseases, such as vascular disease, Alzheimer’s disease, and some cancers. But fatty acids can also help treat diabetes, high blood pressure, and skin conditions.
  • Proper intake is essential for athletes due to the maintenance of the cardiovascular system, but it can also improve respiratory function and prevent asthma.
  • It helps the development of the fetus and reduces the incidence of preterm birth. It has a role in developing good visual acuity and mental development in infants.
  • Lower blood cholesterol levels, reducing the risk of atherosclerosis and heart attack.
  • It plays a role in the transport of fats, and the formation of anti-inflammatory prostaglandins, and their beneficial effects on the immune system are also known. And are involved in the structure of the nervous system and cell membranes.
  • Recent research has shown that children consuming omega-3 fatty acids regularly have improved their task-solving and problem-solving skills to understand tasks faster and improve school performance. Achieving optimal intake by children up to 14 is extremely important, as children’s brains develop to the greatest extent by the time they reach this age.
  • Omega 3 prevents the development of kidney stones

 

Other benefits of fish oil according to health problems:

Aging processes

Slows down the aging process.

Cardiovascular system
  • counteracts arrhythmia symptoms.
  • prevents tachycardia.
  • makes it easier to prevent atherosclerosis.
  • Prevents the development of cardiovascular disease.
  • improves heart function.
  • reduces elevated hematocrit levels.
  • lowers blood pressure in hypertensive patients.
  • reduces the development of Raynaud’s disease.
Digestive system
  • reduces the number of relapsing Crohn’s diseases.
  • prevents the formation of gallstones.
Eyes / vision
  • Fish oil prevents the development of macular degeneration (ARMD) in old age.
  • In the case of dry eyes, fish oil is effective in tear production.
  • In people with wolf blindness, fish oil can improve vision in the dark.
  • Fish oil is easy for the development and treatment of retinopathy.
Immune system
  • Children of women who consume fish oil during pregnancy have a lower rate of allergy.
  • Regular consumption of fish oil to avoid the development of autoimmune diseases.
  • Fish oil prevents the development of certain cancers.
  • It has an anti-inflammatory effect on fish oil.
Metabolism
  • enhances athletic performance.
  • reduces the absorption of cholesterol. Fish oil protects muscle fibers from toxic effects (catabolism).
  • prevents tired formation.
  • prevents the development of insulin resistance.
  • helps break down adipose tissue.
  • lowers triglyceride levels.
Musculoskeletal system
  •  reduces back pain.
  •  promotes bone formation.
  •  protects the muscles from the breakdown (catabolism).
  •  Fish oil is an option for the treatment of polymyalgia rheumatica.
  •  relieves the symptoms of rheumatoid arthritis.
Nervous system
  • reduces aggression.
  • have a beneficial effect on the behavior of patients with hyperactivity.
  • prevent the development of Alzheimer’s disease.
  • relieves depression.
  • has the potential for recovery after head injuries.
  •  improves learning ability.
  •  improves memory.
  •  relieves migraine symptoms.
  •  has the potential to relieve the symptoms of Multiple Sclerosis.
  •  is commonly used in the development of Parkinson’s disease.
  •  is used for schizophrenia.
  •  may be suitable for recovery from spinal cord injuries.
  •  alleviates the toxic effects of mental stress.
Respiratory system
  • may be useful in the treatment of acute respiratory distress syndrome (ARSD).
  •  improves respiratory function in asthmatic patients
  • prevents chronic lung disease.
  • easily prevents the development of bronchitis.
  • prevents emphysema.
  • easily improves lung function and reduce the risk of damage from smoking.
Hormanal problems
  • easily relieves menstrual cramps.
  •  reduces the heat waves associated with menopause and relieve depression.
  •  reduces the risk of developing male infertility.
Skin
  • reduces acne sufferers.
  • relieves the symptoms of eczema.
  • relieves itchy skin.
  • improves skin elasticity.
  • easily prevents sunburn in sensitive people.
  • speeds up wound healing.
Resources
[1]

Wijendran V, Huang MC, Diau GY, et al. Efficacy of dietary arachidonic acid provided as triglyceride or phospholipid as substrates for brain arachidonic acid accretion in baboon neonates. Pediatr Res 2002;51:265-272.

[2]

Goustard-Langelier B, Guesnet P, Durand G,et al. n-3 and n-6 fatty acid enrichment by dietary $sh oil and phospholipid sources in brain cortical areas and nonneural tissues of formula-fed piglets. Lipids 1999;34:5-16.

[3]

Maki KC, Reeves MS, Farmer M, et al. Krill oil supplementation increases plasma concentrations of eicosapentaenoic and docosahexaenoic acids in overweight and obese men and women. Nutr Res 2009;29:609-615.

[4]

Bunea R, El Farrah K, Deutsch L. Evaluation of the effects of Neptune Krill Oil on the clinical course of hyperlipidemia. Altern Med Rev 2004:9:420-428.

[5]

Sampalis F, Bunea R, Pelland MF, et al. Evaluation of the effects of Neptune Krill Oil on the management of premenstrual syndrome and dysmenorrhea. Altern Med Rev 2003;8:171-179.

[6]

Deutsch L. Evaluation of the effect of Neptune Krill Oil on chronic inflammation and arthritic symptoms. J Am Coll Nutr 2007:26:39-48.

[7]

Chang JP, Chen YT, Su KP. Omega-3 polyunsaturated fatty acids (n-3 PUFAs) in cardiovascular diseases (CVDs) and depression: Cardiovasc Psychiatry Neurol 2009;2009:725310. Epub 2009 Sep 27.

[8]

Breslow J. n-3 fatty acids and cardiovascular disease. Am J Clin Nutr 2006;83:1477S-1482S.

[9]

Calzolari I, Fumagalli S, Marchionni N, DiBari M. Polyunsaturated fatty acids and cardiovascular disease. Curr Pharm Des 2009;15:4094-4102.

[10]

No authors listed. Phosphatidylcholine. Altern Med Rev 2002;7:150-154.

[11]

Naguib YM. Antioxidant activities of astaxanthin and related carotenoids. J Agric Food Chem 2000;48:1150-1154.

[12]

Tso P, Drake DS, Black DD, Sabesin SM. Evidence for separate pathways of chylomicron and very low-density lipoprotein assembly and transport by rat small intestine. Am J Physiol 1984;247:G599-G610.

[13]

Amate L, Gil A, Ramirez M. Feeding infant piglets formula with long-chain polyunsaturated fatty acids as triacylglycerols or phospholipids influences the distribution of these fatty acids in plasma lipoprotein fractions. J Nutr 2001;131:1250-1255.

[14]

Tandy S, Chung RW, Wat E, et al. Dietary krill oil supplementation reduces hepatic osteatosis, glycemia, and hypercholesterolemia in high-fat-fed mice. J Agric Food Chem 2009;57:9339-9345.

[15]

Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th ed. New York, NY: Garland Science; 2002.

[16]

Else PL, Hulbert AJ. Membranes as metabolic pacemakers. Clin Exp Pharmacol Physiol 2003;30:559-564

[17]

Kidd PM. Omega-3 DHA and EPA for cognition, behavior, and mood: clinical findings and structural-functional synergies with cell membrane phospholipids. Altern Med Rev. 2007 Sep;12(3):207-27.

[18]

Konagai C, Yanagimoto K, Hayamizu K, Han L, Tsuji T, Koga Y. Effects of krill oil containing n-3 polyunsaturated fatty acids in phospholipid form on human brain function: a randomized controlled trial in healthy elderly volunteers. Clin Interv Aging. 2013;8:1247-57.

[19]

Ebrahimi M, Ghayour-Mobarhan M, Rezaiean S, et al. Omega-3 fatty acid supplements improve the cardiovascular risk profile of subjects with metabolic syndrome, including markers of inflammation and auto-immunity. Acta Cardiol. 2009 Jun;64(3):321-7.

[20]

Derosa G, Cicero AF, Fogari E, et al. Effects of n-3 PUFAs on postprandial variation of metalloproteinases, and inflammatory and insulin resistance parameters in dyslipidemic patients: evaluation with euglycemic clamp and oral fat load. J Clin Lipidol. 2012 Nov-Dec;6(6):553-64.

[21]

Spencer M, Finlin BS, Unal R, et al. Omega-3 fatty acids reduce adipose tissue macrophages in human subjects with insulin resistance. Diabetes. 2013 May;62(5):1709-17.

[22]

Yan Y, Jiang W, Spinetti T, et al. Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation. Immunity. 2013 Jun 27;38(6):1154-63.

[23]

Valensa. FlexPro MD Clinical Trial Overview and Results. (Data on File.) 2011

[24]

McCann JC, Ames BN. Is docosahexaenoic acid, an n-3 long-chain polyunsaturated fatty acid, required for development of normal brain function? An overview of evidence from cognitive and behavioral tests in humans and animals. Am J Clin Nutr 2005;82:281-295.

[25]

Stevens LJ, Zentall SS, Abate ML, et al. Omega-3 fatty acids in boys with behavior, learning, and health problems. Physiol Behav 1996;59:915-920.

    OrganiClinic
    Powered by  GDPR Cookie Compliance
    Privacy Overview

    This website uses cookies so that we can provide you with the best user experience possible. Cookie information is stored in your browser and performs functions such as recognising you when you return to our website and helping our team to understand which sections of the website you find most interesting and useful.