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3. Fatty Acids, Probiotics, and More for ADHD

3. Fatty Acids, Probiotics, and More for ADHD

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Lipid metabolism in ADHD is characterized by altered levels of various fatty acids, with patients exhibiting different lipid and fatty acid profiles.1
MPH and ATX influence ADHD symptoms, among other things, through lipid metabolism2, in different ways3.
A study found no changes in lipid metabolism in ADHD.4

3. Fatty Acids and ADHD

A deficiency of polyunsaturated fatty acids in the blood serum of children with ADHD persisted into adulthood.5 ADHD symptoms in adults correlated with elevated levels of saturated fatty acids containing stearic acid and monounsaturated fatty acids.5

3.1. Polyunsaturated fatty acids

ADHD was associated with lower levels of polyunsaturated fatty acids (PUFAs).67
A review recommended a combination of EPA, DHA, and GLA in a 9:3:1 ratio for ADHD.8 The lead author has a financial interest in a company that sells unsaturated fatty acids.

Rats that were fed a high-fat diet enriched with omega-3 fatty acids during lactation after the mother had been fed a high-fat diet enriched with omega-6 fatty acids during pregnancy, developed microcephaly (small head circumference) with reduced GLUT3 concentrations in the brain.9

3.1.1. Omega-3 fatty acids

Omega-3 PUFAs are not synthesized by the human body and must be obtained through the diet. If your diet is unbalanced, you’ll need to take supplements. Foods high in omega-3 PUFAs include flaxseed oil, flaxseeds, chia seeds, walnut oil, walnuts, canola oil, tuna, herring, salmon, and mackerel.
The need for omega-3 PUFAs is particularly high during growth phases (the first years of life and puberty).
Omega-3 PUFAs are important for the anatomical and functional development of the brain. They influence the maturation and function of neurons, as well as the processes of neurogenesis, migration, synaptogenesis, and neurotransmission. They serve as substrates for the synthesis of bioactive compounds and are involved in the control of acute and chronic inflammation and the regulation of immune cells.10

Omega-3 fatty acids include, among others:

  • Eicosapentaenoic acid (EPA)
  • Docosahexaenoic acid (DHA)
    • A combination of the triple-unsaturated fatty acids EPA and DHA in rats undergoing stress tests11
      • Prevented or compensated for dendritic atrophy in the hippocampal CA3 region
      • Restored GABA release in the hippocampal CA1 region
      • Improved spatial memory.
  • Roughanic acid
  • Alpha-linolenic acid
  • Stearidonic acid
  • Eicosatetraenoic acid
  • Heneicosapentaenoic acid
  • Docosapentaenoic acid
  • Tetracosapentaenoic acid
    (Scoliodonic acid)
  • Tetracosahaxaenoic acid
    (Nisinic acid)

Clinically relevant long-term fat stores are determined based on the erythrocyte membrane (from EDTA-treated blood). Plasma fatty acid analysis, on the other hand, only determines the current daily intake.12

3.1.1.1. Omega-3 Fatty Acids and ADHD

Omega-3 fatty acids are correlated with ADHD symptoms

  • in serum (daily supply)
    • A review of two meta-analyses found:13
      • reduced blood levels of omega-3 (k = 9, N = 586)
      • Improvement in ADHD symptoms following omega-3 supplementation (k = 16, N = 1,408) with a small effect size (SMD ; Hedges’ g = 0.26) on hyperactivity (as rated by teachers and parents) and inattention (as rated only by parents, not by teachers)
    • reduced14, which correlated with increased ADHD symptoms1516
    • no change in ADHD17
    • Alpha-linolenic acid
      • decreased in plasma18
    • Docosahexaenoic acid (DHA)
      • reduced; with no correlation to ADHD symptoms5
      • significantly reduced19
      • elevated in plasma18
    • Eicosapentaenoic acid (EPA)
      • significantly reduced19
      • elevated in plasma18
  • in erythrocyte membranes (long-term supply)
    • reduces14,
    • Docosahexaenoic acid reduces20
3.1.1.2. Omega-3 Fatty Acid Supplementation for ADHD

A review of two meta-analyses found a small ((SMD according to Hedges’ g = 0.26)) improvement in ADHD symptoms following omega-3 supplementation (k = 16, N = 1,408) with regard to hyperactivity (teacher and parent ratings) and inattention (parent ratings only, not teacher ratings).13
A meta-analysis of k = 7 studies involving N = 926 participants found a slight, statistically insignificant improvement in ADHD symptoms following omega-3 supplementation alone.21
A dose of 635 mg of eicosapentaenoic acid (EPA) and 195 mg of docosahexaenoic acid (DHA) (unsaturated fatty acids) reduced serum CRP and IL-6 levels in children with ADHD within 8 weeks in a double-blind, placebo-controlled study and improved ADHD symptoms.22

A combination of the triple-unsaturated fatty acids EPA and DHA in rats undergoing stress tests11

  • Prevented or compensated for dendritic atrophy in the CA3 region of the hippocampus
  • Restored GABA release in the CA1 region of the hippocampus
  • Improved spatial memory.

A placebo-controlled, double-blind study found that omega-3 fatty acids improved attention in children with ADHD as well as in children without the condition.23
A study of healthy adolescents found that consuming walnuts over a 6-month period led to a tendency toward improvement in sustained attention and ADHD symptoms among those participants who consumed nuts more consistently.24 This could indicate that adolescents who perceive a benefit (even if unconscious) from consuming walnuts are more likely to continue doing so.

A double-blind, placebo-controlled study found that DHA did not improve ADHD symptoms.25

Conclusion: Omega-3 fatty acid supplementation may have a beneficial effect. The achievable effect size of 0.26 is too low to detect an improvement in an individual. Below an effect size of 0.5, an improvement can only be detected statistically within a group. Therefore, treating ADHD with omega-3 fatty acids alone is unlikely to be effective.

3.1.2. Omega-6 fatty acids

Omega-6 fatty acids include, among others:

  • Arachidonic acid (AA)
  • Linoleic acid (LA)
  • Gamma-linolenic acid (GLA)
  • Dihomo-gamma-linolenic acid (DHGLA)
  • Adrenic acid
3.1.2.1. Omega-6 Fatty Acids and ADHD
  • Omega-6 fatty acids and ADHD:
    • in serum (daily supply)
      • increased15, which correlated with increased ADHD symptoms1617
      • Arachidonic acid
        • reduced; no correlation with ADHD symptoms5
        • significantly reduced19
      • Reduced levels of dihomogammalinoleic acid; no correlation with ADHD symptoms5
      • Increased adrenic acid17
      • Gamma-linolenic acid (GLA) increases17
    • in erythrocyte membranes (long-term supply)
      • Gamma-linolenic acid (GLA) increases20
      • Arachidonic acid reduces20
3.1.2.2. Omega-6 Fatty Acid Supplementation for ADHD

One RCT found no improvement in the ADHD-RS intention-to-treat score or in inattention following omega-3/6 supplementation at either 6 or 12 months. A positive response was observed in 46.3% of the omega-3/6 group and 45.6% of the placebo group. The study used two capsules daily, each containing 279 mg of eicosapentaenoic acid [EPA], 87 mg of docosahexaenoic acid [DHA], and 30 mg of gamma-linolenic acid [GLA].26

Conclusion: Omega-6 fatty acid supplementation has no effect on ADHD. Administration of omega-6 fatty acids (with the exception of arachidonic acid) may actually tend to have an adverse effect.

3.1.3. Omega-3 and Omega-6 Fatty Acid Supplementation for ADHD

A double-blind RCT involving 41 children with ADHD and learning disabilities found improvements following daily administration of EPA (186 mg), DHA (480 mg), gamma-linolenic acid (96 mg), vitamin E (as DL-alpha-tocopherol, 60 IU), cis-linoleic acid (864 mg), AA (42 mg), and thyme oil (8 mg). The placebo group received olive oil.27
One RCT found no improvement in the ADHD-RS intention-to-treat score or in inattention following omega-3/6 supplementation at either 6 or 12 months. A positive response was observed in 46.3% of the omega-3/6 group and 45.6% of the placebo group. The study used two capsules daily, each containing 279 mg of eicosapentaenoic acid [EPA], 87 mg of docosahexaenoic acid [DHA], and 30 mg of gamma-linolenic acid [GLA].26
.

3.2. Monounsaturated fatty acids

A study based on genetic analyses found no evidence of a causal link between unsaturated fatty acids and ADHD.28
A study found no changes in serum levels in patients with ADHD.17
Two very small studies found elevated levels of monounsaturated fatty acids in ADHD:

  • Omega-7 fatty acids
    • Elevated serum palmitoleic acid levels, with no correlation to ADHD symptoms5
  • Omega-9 fatty acids
    • Nervonic acid (found at reduced levels in erythrocyte membranes, which reflect long-term supply for ADHD)20
    • oleic acid
      • elevated in erythrocyte membranes, which reflect long-term supply)20
      • increased without any correlation to ADHD symptoms5
      • decreased in plasma18

3.3. Saturated fatty acids

A large study of 432 children found significantly higher serum levels of saturated fatty acids in children with ADHD.29 This correlated with a higher intake of nutrient-poor foods—such as those high in sugar and fat—and a lower intake of vegetables, fruits, and protein-rich foods compared to healthy children. It remains unclear whether the dietary changes are a cause, a consequence, or part of a vicious cycle.
Another study also found elevated levels of saturated fatty acids in the blood (daily intake) and in erythrocyte membranes (long-term intake) 14,
A study found no changes in serum levels in patients with ADHD.17

3.4. Fatty Acid-Binding Proteins

Fatty acid-binding proteins (FABPs) are small cytoplasmic proteins that play a role in cellular lipid metabolism by taking up and transporting hydrophobic substances—such as fatty acids, cholesterol, and retinoids—within the cell. Among other things, they transport long-chain polyunsaturated fatty acids (PUFAs), which are essential for brain development and neurotransmission.30

FABPs may be the primary targets of endocannabinoid transport inhibitors such as AM404, VDM-11, LY-2183240, URB597, AM1172, O-2093, OMDM-2, UCM-707, guineensin, WOBE437, and RX-055, and thus play a key role in the effects these compounds mediate in vivo, such as the regulation of pain, inflammation, neuroprotection, and neuronal signaling.31

Subtypes:

  • FABP1 (not shown here)
  • FABP2 (not shown here)
  • FABP330
    • Other names: Fatty acid-binding protein 3, H-FABP, M-FABP (Muscle Fatty Acid-Binding Protein), MDGI (Mammary-derived growth inhibitor), O-FABP (Cardiac fatty acid-binding protein), FABP11
    • In the brain
      • In
        • Hippocampus
        • Reaction flask
        • Cerebellum
        • Thalamus
        • Hypothalamus
        • Caudate Nucleus
      • In the cytoplasm
      • In neuronal nuclei
      • Activation of nuclear receptors
        • FABP3 preferentially transports ligands to PPARα31
      • Associated more with functional signaling processes than with long-term structural changes
    • Ligands
      • High affinity for epoxyicosatrienoic acids (endocannabinoids derived from arachidonic acid)
      • Arachidonic acid: Ki 0.0331
      • AEA: Ki 3.0731
      • OEA: Ki 4.6931
    • FABP3 binds to D2R and regulates D2R3230
  • FABP4 (not shown here)
  • FABP530
    • Other names: Fatty acid-binding protein 7, Epidermal fatty acid-binding protein 5 (E-FABP), Psoriasis-associated fatty acid-binding protein (PA-FABP), Epidermal-type fatty acid-binding protein
    • In the brain in
      • Hippocampus
      • Reaction flask
      • Cerebellum
      • Thalamus
      • Hypothalamus
      • Caudate Nucleus
      • Amygdala
      • Cerebral Cortex
      • Corpus callosum
      • Retina
      • Lens
      • In neurons and glial cells
        • At Soma
        • In the cores
        • In the appendices
    • Features
      • Key Role in Early Development
        • Involved in neuronal cell differentiation
        • Involved in neurite growth
      • Highest expression in prenatal and early postnatal neurons
      • Associated more with functional signaling processes than with long-term structural changes
      • Activation of nuclear receptors
        • PPAR3331
        • FABP5 enhances the activation of PPARβ/δ31
        • RXR30
      • FABP5 protects against 6-OHDA-induced Parkinson’s disease via the PPARγ/SIRT1/PGC-1α signaling pathway34
      • A key role in the regulation of central endocannabinoid signaling
        • At glutamatergic synapses35
        • Reduces AEA33
        • FABP5 deletion36
          • Increases AEA in the striatum, prefrontal cortex, midbrain, and thalamus
          • Increases 2-AG in the midbrain
          • Impaired tonic 2-AG and AEA signaling at GABAergic synapses of medium spiny neurons in the striatum
          • Reduced phasic 2-AG-mediated short-term synaptic plasticity
          • Left CB1R expression and function unchanged
        • FABP5 deletion in astrocytes, but not in neurons37
          • Blocked the 2-AG-mediated depolarization-induced suppression of inhibition in the hippocampus
    • FABP5 and Dopamine
      • FABP5 facilitates the uptake of DHA into the brain through the blood-brain barrier38
        • The PPARγ agonist pioglitazone increased FABP5 expression and DHA uptake into the brain39
      • DHA appears to facilitate dopamine transport40
      • DHA deficiency in the brains of female rats reduced D2-like receptors in the ventral striatum and increased D1-like receptors in the caudate nucleus41
    • Ligands
      • High affinity for epoxyicosatrienoic acids (endocannabinoids derived from arachidonic acid)
      • Are presumably closely linked to disorders associated with altered neurotransmission
      • Arachidonic acid: Ki 0.1231
      • AM404: Ki 0.3931
      • AM1172: Ki 0.4931
      • GW7647; Ki 0.7031
      • BMS309403: Ki 0.8931
      • AEA: Ki 1.2631
      • VDM11: Ki 1.7531
      • OEA: Ki 2.2231
      • OMDM1: Ki 2.6731
      • OMDM2: Ki 3.8531
  • FABP6 (not shown here)
  • FABP730
    • Other names: Fatty acid-binding protein 7, B-FABP, Brain-type fatty acid-binding protein, Brain lipid-binding protein (BLBP), Mammary-derived growth inhibitor-related
    • In the brain in
      • Hippocampus
      • Reaction flask
      • Cerebellum
      • Thalamus
      • Hypothalamus
      • Amygdala
      • Cerebral Cortex
      • Corpus callosum
      • Radial glial cells and immature astrocytes
        • In the cytoplasm
        • At its core
    • Features
      • PUFA Metabolism
      • Neural migration
      • Development of neural progenitor cells
      • Pattern Formation of the Neural Axis
      • Sleep
      • A clock-controlled gene involved in sleep-wake regulation
      • Metabolic function
      • Potentially involved in developmental disorders and neurodegeneration
      • Associated more with long-term structural changes than with functional signaling processes
    • Ligands
      • At body temperature, there is no strong preference for any particular type of fatty acid
      • When bound to docosahexaenoic acid
        • Localization of FABP7 in the cell nucleus
        • Influencing Gene Expression
      • Arachidonic acid: Ki 0.0931
      • AEA: Ki 0.8031
      • OEA: Ki 0.3531
    • FABP7 deletion causes30
      • Abnormal dendritic morphology
      • Reduced density of dendritic spines in astrocytes and cortical pyramidal neurons
      • Reduced number of excitatory synapses in the mPFC
      • Reduced frequency and amplitude of excitatory postsynaptic miniature currents
      • Reduced cerebral glucose metabolism in the striatum, cortex, hypothalamus, and amygdala
      • Increased cerebral glucose metabolism in the hippocampus, thalamus, periaqueductal gray matter, superior colliculi, inferior colliculi, cerebellum, and midbrain
      • Anxiety-like behaviors, enhanced anxiety memory, and lower brain DHA levels during the neonatal period in FABP7 null-mutant mice42
    • FABP7 expression fluctuates in accordance with the circadian rhythm
    • FABP7 upregulation in the PFC is thought to correlate with the severity of autism43
  • FABP8 (not shown here)
  • FABP9 (not shown here)

Changes in FABP expression and PUFAs in the brain affect key regulatory proteins and signaling pathways, such as peroxisome proliferator-activated receptors (PPARs) and retinoid X receptors (RXRs).

4. Low-Density Lipoprotein

A study found significantly elevated blood levels of total cholesterol and low-density lipoprotein (LDL) in children with ADHD, while high-density lipoprotein (HDL) and triglyceride (TG) levels did not differ from those of people with ADHD.44 In contrast, another study found significantly lower blood levels of total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) in boys with ADHD (regardless of subtype).45
In a large cohort study of adults, a slight decrease in low-density lipoprotein (LDL) levels was observed.46
A KIGGS study found no differences in serum lipid parameters between the ADHD group (n = 1,219) and the control group (n = 9,741)—neither in total cholesterol, LDL, HDL, nor triglycerides—neither at baseline nor at the 10-year follow-up—even when MPH use was taken into account.47

Treatment of adults with bipolar disorder and comorbid ADHD using lisdexamfetamine (Vyvanse) resulted in a significant decrease in weight, body mass index, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol, but not in triglycerides or blood glucose levels.48

A study suggests a genetic mutation in the low-density lipoprotein receptor in ADHD.49
Elevated serum LDL cholesterol, with no correlation to ADHD symptoms
Another small study also found that lipoprotein metabolism is altered in ADHD.50

Among other things, methylphenidate lowers low-density lipoprotein levels.51

Further studies on fats and fatty acids in ADHD did not yield any clear results.52

5. Sphingolipids

Sphingolipids are essential lipids derived from the amino alcohol sphingosine.
They serve as structural components of cell membranes, particularly in nervous tissue. They stabilize lipid rafts, act as signaling molecules, and, as components of the skin barrier, strengthen its protective function. The most important classes include ceramides, sphingomyelins, and glycosphingolipids.

SHR showed significantly elevated levels of gangliosides and lysophospholipids in the PFC.53
Intraperitoneal administration of the SPHK inhibitor SKI II (15 mg/kg, 16 days)

  • specifically reduced the sphingomyelin content.
  • increased the mRNA and protein expression of SPHK1 and SPHK2, in parallel with increased S1P levels
  • selectively reduced Sphk2 mRNA expression (without altering protein levels)
  • significantly improved hyperactivity, impulsivity, and anxiety-like behavior
  • restored dopamine β-hydroxylase expression

6. Treatment of the Gut-Brain Axis in ADHD

6.1. Probiotics for ADHD

For background information on gut bacteria, the gut-brain axis, and their role in the development of ADHD, see Gut Bacteria, Gut-Brain Axis In the article Age-Independent Physical Stress as an Environmental Cause of ADHD in the chapter “Development.”

Various studies report positive effects of probiotics in children with ADHD.

  • L. rhamnosus GG
    • Administration during the first 6 months of life reduced the risk of ADHD later in life54
    • Administration to children improved ADHD symptoms as rated by parents, but not as rated by teachers55
  • Bacteroidetes bifidum Bf-688
    • Administration to children improved inattention, hyperactivity/impulsivity, and increased weight5657
      • Firmicutes reduced
      • The ratio of Firmicutes to Bacteroidetes (F/B ratio) is reduced
      • Proteobacteria increased
      • Improved neuropsychological performance (when co-administered with MPH)
      • reduced N-glycan biosynthesis (when co-administered with MPH)
      • Significant improvement in omission errors on the CPT (when MPH is co-administered)
      • Significant improvement in hit reaction time on the CPT and CATA (when co-administered with MPH)
    • Administration of Bacteroidetes bifidum BD1 to newborn female SHR rats (109 CFU daily via a nasogastric tube for 3 weeks) resulted in the following after 7 weeks58
      • significantly reduces congenital hyperactivity
      • Elevated levels of DAT and tyrosine hydroxylase in the striatum
      • significantly reduced the number of activated microglia
      • Significantly elevated levels of Treg cells in the spleen
      • Improved α-diversity in the gut microbiota
      • Decreased Firmicutes/Bacteroidota ratio
      • Muribaculaceae increased
      • Proliferation of Clostridia_UCG-014 is suppressed
    • Bifidobacterium bifidum TMC3115, in combination with 2’-fucosyllactose (2’-FL), caused the following in female newborn SHR rats:59
      • Reduced hyperactivity
      • Increased expression of tyrosine hydroxylase and the dopamine transporter in the striatum
      • Increased diversity of the gut microbiota
      • Bacillus and Turicibacter reduced
  • B. subtilis, B. bifidum, B. breve, B. infantis, B. longum, L. acidophilus, L. delbrueckii, L. casei, L. plantarum, L. lactis, L. salivarius, S. thermophiles
    • Administration in addition to MPH improved ADHD symptoms in children compared to placebo60
  • L. reuteri, L. acidophilus, L. fermentum, B. bifidum
    • The treatment improved ADHD symptoms in children compared with placebo. In addition, high-sensitivity C-reactive protein (hs-CRP) levels in serum decreased, and total antioxidant capacity (TAC) in plasma increased compared with placebo. CDI and other metabolic markers remained unchanged.61
  • L. mesenteroides, L. paracasei, L. plantarum, beta-glucan, inulin
    • ADHD symptoms improved to the same extent in children and adults in both the treatment group and the placebo group; ASD symptoms remained unchanged62
  • Lactobacillus plantarum PTCC 1896™ (A7), Bifidobacterium animalis subsp. lactis (BB-12®)
    • A significant decrease in total ADHD scores on the CPRS (Connor Parent Rating Scale) after 4 weeks of treatment with MPH plus [placebo] compared to [placebo] plus [ MPH], but this effect was no longer observed after 8 weeks of intervention.63
  • L. helveticus, B. animalis subsp. lactis, Enterococcus faecium, B. longum, Bacillus subtilis64
    • In a double-blind RCT, treatment over 3 months improved hyperactivity and gastrointestinal symptoms and enhanced academic performance
    • Younger participants showed greater improvements
    • Improvements were correlated with lower cortisol levels

A meta-analysis found that probiotics did not improve ADHD symptoms.65

6.2. Fecal Transplantation for ADHD

To date, there have been no studies necessary to assess whether fecal transplants are a treatment option for ADHD.

A study found that mice whose guts were colonized with gut bacteria from people with ADHD exhibited structural changes in the brain (white matter, gray matter, hippocampus, internal capsule), reduced connectivity between the right motor and visual cortices during the resting state, and higher levels of anxiety than mice that were exposed to gut bacteria from people without ADHD.66
A case study reports an improvement in a young woman’s ADHD symptoms following a gut microbiota transplant performed in connection with a recurrent Clostridioides difficile infection.67

7. Additional Resources on ADHD

7.1. Polyphenols

Polyphenols are aromatic compounds with two or more hydroxyl groups directly attached to an aromatic ring. Polyphenols are derived from phenylalanine, which in turn is derived from shikimic acid.

Natural polyphenols (of which there are said to be over 8,000) are often found in plants as bioactive substances (pigments, flavor compounds, tannins), e.g.,

  • Flavonoids (pigments)
    • Flavonoids appear to act as glutamate antagonists and GABA agonists.68
  • Anthocyanins (pigments)
  • Procyanidins
  • Benzoic acid derivatives, e.g.,
    • Vanillic acid
    • Gallic acid
    • Protocatechuic acid
  • Cinnamic acid derivatives, e.g.,
    • Caffeic acid
    • Kumaric acid
  • Stilbene derivatives, e.g.,
    • Resveratrol
      • A component of red wine

Certain polyphenols are believed to be able to influence neurophysiological changes caused by early childhood stress:69 For example:

  • Reduction of depressive symptoms through
    • Xanthohumol
    • Quercetin
    • Phlorotannins
  • Reduction of anxiety symptoms through
    • Quercetin
    • Phlorotannins
  • Reversing the decrease in BDNF by
    • Xanthohumol
  • No reversal of the changes in dopamine and serotonin levels in the brainstem caused by early stress
  • Reduction of the cortisol stress response to acute stress through
    • Xanthohumol

A study found a correlation between increased polyphenol intake and a reduced risk of ADHD in preschoolers.70

7.2. Phosphatidylserine

Phosphatidylserine is not a vitamin, but a phospholipid.

Source: Bieger.71

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