Depression: What are the natural alternatives to antidepressants?

Depression: What are the natural alternatives to antidepressants?

We are not all equal when it comes to depression.


Genetics: Some individuals experience a deficiency in neurotransmitters responsible for maintaining a good mood, or an inability to metabolize a vital vitamin essential for mental well-being.

Diet: It directly influences the body’s ability to produce and regulate the hormones and neurotransmitters that affect our mood.

Elderly people, smokers, drinkers, heavy coffee consumers, and those under chronic stress often experience impaired vitamin absorption over time.

Not all depressions are the same

Mild depression or severe depression? There are different types of depression:

  • Mild depression, also known as "characterized depressive episode":
    • lasting most of the day for at least two weeks.
  • Severe depression (major):
    • is distinguished by the ability—or inability—to perform daily tasks like working, eating, or personal hygiene.
  • An intermediate state, referred to as "moderate depression," is also recognized:
    • where clear signs of depression are present, yet the individual can still manage essential responsibilities.

Symptoms are similar across types. Whether depression is mild, moderate, or severe, common signs include:

“Irritability, low energy and mood even for favorite activities, reduced libido, feelings of despair...” But, why automatically resort to medication designed for severe depression? While denial should be avoided (as it risks escalating into a more severe depressive state), is taking psychotropics truly the right solution for mild or moderate depression?

Antidepressants and Anxiolytics: What Are They Used For?

Addressing a Chemical Imbalance?

Since the 1960s, depression has been treated by addressing a deficiency in serotonin2. People suffering from depression often exhibit a lack of serotonin, a neurotransmitter that also functions as a hormone.

The level of serotonin influences: mood, emotional response, aggression, sexual and eating behaviors, and sleep. It’s no surprise that a drop in serotonin levels can lead to heightened emotions, increased aggression, comfort eating, and significant difficulty achieving restful sleep.

Antidepressants enhance serotonin effects by reducing its reabsorption into the presynaptic neuron.

Are Antidepressants Ineffective? A Divided Scientific Community.

  • Serotonin levels are not the sole chemical factor linked to depression.

Depression is also associated with homocysteine levels, which can be influenced by deficiencies in B vitamins, vitamin D, zinc, and myo-inositol. We’ll explore this further.

  • Antidepressants may act as a placebo for mild to moderate depression.

Research conducted by the British research group led by Professor Irving Kirsch in 20083 revealed that:

Patients with mild, moderate, and severe depression who were given a placebo showed similar improvements to those receiving actual antidepressants.

Notably, this did not apply to patients with the most severe forms of depression. Following significant counterarguments4, Professors Fournier5, Zimmerman, and Thongy (USA)6 confirmed these findings. They also suggested that the observed decline in antidepressant efficacy around the sixth month is due to the placebo effect wearing off.

The Risks of Antidepressants and Anxiolytics

This is not about condemning a medication that can save lives but rather highlighting the dangers of rushing into its use, often considered harmless.

Risks Associated with Antidepressants:

1) Sexual Dysfunction12 linked to SSRIs (Selective Serotonin Reuptake Inhibitors):
- Difficulty achieving orgasm
- Decreased libido
- Erectile dysfunction
- Delayed ejaculation
- Persistent Sexual Dysfunction Syndrome (Post-SSRI Sexual Dysfunction)

2) Psychological Issues
- Repeated anxiety attacks
- Sleep disturbances
- Persistent irritability
- Suicidal thoughts13

3) Manic Risk14
- Hypomania15 (a milder form of mania characterized by unexplained euphoria)

4) Dangerous Combinations
- When combined with opioids (e.g., Codeine or Morphine), the risk of "serotonin syndrome" increases. Symptoms include tremors, hallucinations, excessive sweating, and even coma16.

5) Anxiety, Intense, Sudden Feelings of Panic that may become chronic17

6) Addiction

  • Antidepressant efficacy often declines by the sixth month.
  • An increasing number of patients show resistance to antidepressants7, 8.

=> The only option: intensifying prescriptions with antidepressants, mood stabilizers (e.g., Lithium, Lamotrigine) aimed at "boosting" the effects of the initial psychotropics9, or even electroconvulsive therapy.

Risks Associated with Anxiolytics

Anxiolytics, often prescribed to calm chronic anxiety, do not address true depressive syndromes. However, they are sometimes combined with antidepressants because of their rapid action.

Short-Term Benefits: By reducing communication between nerve cells, they lower anxiety, improve sleep, and relax muscles. The most prescribed in France are benzodiazepines.

Medium- and Long-Term Side Effects:

  • Drowsiness, balance issues, memory impairment, and dependence: beyond 12 weeks of treatment.
  • Risks to the fetus if taken during pregnancy: malformations, low muscle tone, hyperexcitability18.
  • Cognitive Impairments:
    • Short-Term: Attention deficits, learning difficulties, memory issues, and impaired visuo-spatial ability.
    • Effects persisting for months after treatment ends.
    • Long-Term: Irreversible damage such as cases of dementia (though less common)20.

A Growing Awareness
An increasing number of doctors and researchers believe that mild to moderate depression should not systematically lead to prescriptions of antidepressants or anxiolytics21, 22.

Nutrition can help regulate depression

Homocysteine: the cellular toxin linked to depression (among other issues)

Homocysteine: an often-overlooked amino acid that must be carefully monitored. Elevated homocysteine levels are commonly found in individuals with depression, bipolar disorder, and anxious children. 26, 27

Excessive levels are also associated with:

  • Cardiovascular diseases such as hypertension and heart attacks. 23, 24
  • Dementia and Alzheimer's disease. 25

High homocysteine levels can cause poor blood flow to the brain, neurotransmitter deficiencies, and DNA damage. 28, 29

Homocysteine levels increase in cases of vitamin B6, B9, and B12 deficiencies because:

Normally, homocysteine is broken down into methionine through two pathways:

  1. One pathway relies on active forms of vitamin B12 (methylcobalamin) and vitamin B9 (5-methyltetrahydrofolate).
  2. The other takes place in the liver and depends on vitamin B6.

Important: The B6, B9, and B12 vitamins found in food are inactive. Only supplementation with their active forms is effective.

Normally, the body uses enzymes to activate these vitamins. However, many individuals with depression experience enzyme dysfunction, preventing the conversion of inactive folic acid (vitamin B9) into active vitamin B9.

What about other common nutritional deficiencies in depression?

People with depression often exhibit deficiencies in myo-inositol, zinc, and vitamin D3.

  1. Myo-inositol plays a role in signal transmission at the receptors of several neurotransmitters in the prefrontal cerebral cortex. While not the sole cause of depression, adequate levels are essential. 30
  2. Low blood zinc concentrations are linked to depression, which makes sense given zinc's role in regulating nerve impulses. 31
  3. Depressive episodes are also associated with vitamin D deficiency or insufficient sunlight exposure. Proper supplementation can alleviate symptoms. 32

What are natural remedies for mild depression?

  1. Psychotherapy helps identify the impact of emotions and preconceived notions, enabling individuals to gain better mental control.
  2. Hypnosis, particularly EMDR, proves effective, especially when depression is triggered by trauma.
  3. A tailored nutritional supplementation can empower the brain to naturally combat depression.
  4. Lastly, prioritizing sufficient sleep and regular exercise is essential.

How to naturally boost serotonin levels and maintain healthy neurons?

Include foods rich in tryptophan, a precursor of serotonin, such as whole-grain rice, dairy products, eggs, fish, legumes, chocolate, and bananas.

Consume fatty fish rich in omega-3s two to three times a week. Remember, 60% of our brain's structure is composed of fatty acids!

If dietary intake is insufficient, consider marine omega-3 supplements rich in DHA. Opt for pure krill oil, which is 2.5 times more absorbable than fish oil and delivers phospholipids directly to neurons. Avoid synthetic omega-3s (omega-3 esters, which are poorly absorbed).

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What supplementation is needed for nutritional balance?

The goal is to restore the brain's natural defenses to fight depression.

This involves addressing:

  • The serotonin levels through a standardized saffron extract rich in safranal and crocin.
  • The homocysteine levels with active forms of vitamins B6, B9, and B12.
  • Preventing deficiencies in myo-inositol, zinc, and vitamin D3.

SOLAFRAN: A unique and comprehensive supplement that combines:

  • The well-known antidepressant properties of a saffron extract, standardized with safranal and crocin.
  • Myo-inositol.
  • Vitamins B9, B6, B12, and D3, all in their biologically active forms, addressing deficiencies observed in individuals with depressive states.
  • Highly absorbable zinc and turmeric phytosome.

What Makes Our Saffron Extract Unique?

The Solafran (Saffr’Activ™) saffron extract stands out for its precise standardization, containing 3% Safranal and 2% Crocin. These compounds are widely recognized for their anxiety-reducing and anti-cancer properties, among other benefits.

How Does It Work?

Our Saffr’Activ™ extract works on five levels:

Level One: Acts as a natural antidepressant with no side effects

Saffr’Activ enhances the availability of serotonin and norepinephrine. Numerous placebo-controlled studies, including comparisons with well-known antidepressants like Fluoxetine (Prozac) and Imipramine (Tofranil), have confirmed its efficacy.

The results are clear: saffron extract performs just as effectively as traditional antidepressants but without side effects. 33,34,35

Saffron, nature’s treasure, still holds many untapped secrets.

Moreover, if you are currently taking antidepressants, saffron has been shown to help reduce common side effects such as dry mouth, insomnia, irritability, and significantly decreased libido (see above: "risks associated with antidepressants"). 36,37

Level Two: Increases dopamine levels

Maintaining sufficient dopamine levels is vital since this neurotransmitter is the source of pleasure, motivation, and joy. When you enjoy doing or eating something, it’s because your dopamine levels are rising.

Conversely, low dopamine levels can gradually lead to behavioral issues, muscle stiffness, difficulty processing information, and a lack of motivation. No wonder Parkinson’s patients—whose dopamine receptors are affected—often experience depression!

Dopamine also plays a crucial role in supporting heart and kidney function.

Level Three: Boosts natural glutamate levels

Glutamate, an amino acid functioning as a neurotransmitter in the brain, is essential for learning and memory.

Maintaining adequate levels of natural glutamate in the brain is critical.

Why natural?

Because synthetic glutamate, such as monosodium glutamate (MSG), is widely used as a flavor enhancer in the food industry. The body doesn’t recognize this chemical glutamate, and repeated consumption can act as a toxin, leading to migraines, weight gain, muscle pain, gastrointestinal disorders, and even depression.

Level Four: Protects neurons from oxidation

Just like other cells in our body, neurons need protection from oxidative damage.

Level Five: Lowers homocysteine levels

A double-blind, placebo-controlled study demonstrated that a standardized saffron extract can significantly lower homocysteine levels. 38

What Are the Other Effects of Our Saffron Extract?

In a double-blind, placebo-controlled study, 100% of participants reported improved sleep quality.

The saffr’activ extract demonstrated in a 2014 study a direct impact on sleep: all participants experienced faster sleep onset and improved overall sleep quality scores.

This effect was noticeable within 20 days of treatment and further enhanced after 40 days.

A meta-analysis of 12 placebo-controlled studies highlighted the benefits of standardized saffron not only for mild to moderate depression but also for sexual dysfunction, infertility, and as a remarkable aid in curbing excessive eating behaviors. 39

Vitamins B6, B9, and B12 to Reduce Homocysteine Levels

Solafran contains the active forms of these vitamins, making them immediately bioavailable. Each capsule delivers 3 mg of active vitamin B6 (pyridoxal-5-phosphate), providing 214% of the RDI, 100 µg of active vitamin B9 (L-methylfolate), providing 50% of the RDI, and 75 µg of active vitamin B12 (methylcobalamin), offering a remarkable 3000% of the RDI for optimal rebalancing!

These three vitamins work synergistically to naturally regulate homocysteine levels.

Myo-Inositol, Zinc, and Vitamin D3 in Optimal Quantities

Solafran also includes 75 mg of myo-inositol, 2 mg of highly bioavailable zinc (mono-L-methionine sulfate), and even 12 µg of vitamin D3.

Turmeric Phytosome

Curcumin exhibits natural antidepressant properties, shown to be as effective as certain medications (fluoxetine) in studies on patients with moderate depression. 40

Turmeric phytosome is also well-recognized as the most extensively studied form of curcumin for combating inflammation.

Each Solafran capsule contains 160 mg of turmeric phytosome.

What Can You Expect from Solafran?

Solafran helps naturally and deeply restore balance to the mechanisms that lead to low moods and improve sleep quality, without addiction or side effects.

Solafran can support you in the following ways:

  • Helping to overcome mild to moderate depression, regardless of its cause,
  • Complementing psychotherapy,
  • Reducing the side effects of traditional antidepressants,
  • Improving sleep quality during periods of stress or anxiety.

It also has antioxidant properties and may help prevent neurodegenerative diseases.

Depending on your condition, the effects can be noticeable quite quickly. However, if deficiencies are significant, it may take two to three months for some individuals to experience full benefits.

How Many Capsules per Day? Is It Expensive?

Only one vegetable capsule per day is required.

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Is There Any Risk in Taking Solafran?

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Scientific Studies:

1 Stockholm: Swedish Council on Health Technology Assessment (SBU). Treatment of Depression: A Systematic Review; 2004 Mar. SBU Yellow Report No. 166/1+2+3  
2  Rachel Roberts, Depression the leading cause of ill health and disability worldwide, who finds, The Independant, 2017 March.
3 Stockholm: Swedish Council on Health Technology Assessment (SBU). Treatment of Depression: A Systematic Review; 2004 Mar. SBU Yellow Report No. 166/1+2+3     
4  Barbosa L., Berk M., Vorster M.,  A double-blind, randomized, placebo-controlled trial of augmentation with lamotrigine or placebo in patients concomitantly treated with fluoxetine for resistant major depressive épisodes, J Clin Psychiatry. 2003 Apr;64(4):403-7.
6  Jay C. Fournier, MA; Robert J. DeRubeis, PhD; Steven D. Hollon, PhD; et al , Antidepressant Drug Effects and Depression SeverityA Patient-Level Meta-analysis, JAMA.  2010;303(1):47-53. doi:10.1001/jama.2009.1943 
7  Zimmerman M. Thongy T.,  How often do SSRIs and other new-generation antidepressants lose their effect during continuation treatment? Evidence suggesting the rate of true tachyphylaxis during continuation treatment is low, J Clin Psychiatry. 2007 Aug;68(8):1271-6.
8 Zimmerman M., Posternak MA., Chelminski I., Symptom severity and exclusion from antidepressant efficacy trials.J Clin Psychopharmacol. 2002 Dec;22(6):610-4.
9 Rush AJ, Trivedi M., Fava M., Depression, IV: STAR*D treatment trial for depression, Am J Psychiatry. 2003 Feb;160(2):237
10 American College of Obstetricians and Gynecologists (ACOG). Use of psychiatric medications during pregnancy and lactation. Washington (DC): American College of Obstetricians and Gynecologists (ACOG); 2008 Apr. 20 p
11Mezzacappa A, Lasica PA, Gianfagna F, Cazas O, Hardy P, Falissard B, Sutter-Dallay AL, Gressier F, Risk for Autism Spectrum Disorders According to Period of Prenatal Antidepressant Exposure: A Systematic Review and Meta-analysis, JAMA Pediatr. 2017 Jun 1;171(6):555-563. doi: 10.1001/jamapediatrics.2017.0124
12  Csoka AB, Bahrick A, Mehtonen OP, Persistent sexual dysfunction after discontinuation of selective serotonin reuptake inhibitors, J Sex Med. 2008 Jan;5(1):227-33
13 Bridge JA, Iyengar S, Salary CB, Barbe RP, Birmaher B, Pincus HA, Ren L, Brent DA, MD. Clinical Response and Risk for Reported Suicidal Ideation and Suicide Attempts in Pediatric Antidepressant Treatment: A Meta-analysis of Randomized Controlled Trials. JAMA. 2007;297:1683-1696.
14 Christophe Bagot, "Hypomanie et Manie".
15  Joseph MF, Youngstrom EA, Soares JC, Antidepressant-coincident mania in children and adolescents treated with selective serotonin reuptake inhibitors, Future Neurol. 2009 Jan 1;4(1):87-102
16  Solhaug V., Molden E., Individual variability in clinical effect and tolerability of opioid analgesics - Importance of drug interactions and pharmacogenetics, Scand J Pain. 2017 Oct 17;17:193-200
17  Marcinkiewcz CA, Mazzone CM, D'Agostino G, Halladay LR, Hardaway JA, DiBerto JF, Navarro M, Burnham N, Cristiano C, Dorrier CE, Tipton GJ, Ramakrishnan C, Kozicz T, Deisseroth K, Thiele TE, McElligott ZA, Holmes A, Heisler LK, Kash TL, Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala, Nature. 2016 Sep 1;537(7618):97-101
18  Ronit Calderon-Margalit, MD, MPH, Chunfang Qiu, MD, MS, Asher Ornoy, MD, David Siscovick, MD, MPH, and Michelle A. Williams, Risk of Preterm Delivery and Other Adverse Perinatal Outcomes in Relation to Maternal use of Psychotropic Medications during Pregnancy, Am J Obstet Gynecol. 2009 Dec; 201(6): 579.e1–579.e8. 
19 Melinda JBarkerKenneth MGreenwoodMartinJacksonSimon FCrowe, Persistence of cognitive effects after withdrawal from long-term benzodiazepine use: a meta-analysis, Archives of Clinical Neurobiology, Volume 19, Issue 3, April 2004, Pages 437-454
20 GuoChao Zhong,,Yi Wang, Yong Zhang, and Yong Zhao, Association between Benzodiazepine Use and Dementia: A Meta-Analysis, PLoS One. 2015; 10
21 Irving Kirsch, Response Expectancy and the Response to Antidepressant Medication, Elsevier B.V., 2017, Oct.,/1+2
22  Mc Allister-Williams RH, Do antidepressants work? A commentary on "Initial severity and antidepressant benefits: a meta-analysis of data submitted to the Food and Drug Administration" by Kirsch et al., Evid Based Ment Health. 2008 Aug;11(3):66-8
23 Fanapour PC, Yug B, Kochar MS. Hyperhomocysteinemia: an additional cardiovascular risk factor. WMJ. 1999 Dec;98(8):51-4. Review. PubMed PMID: 10639897.
24 van Beynum IM, Smeitink JA, den Heijer M, te Poele Pothoff MT, Blom HJ. Hyperhomocysteinemia: a risk factor for ischemic stroke in children. Circulation. 1999 Apr 27;99(16):2070-2. PubMed PMID: 10217643.
25 SESHADRI, Sudha, et al. Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. New England Journal of Medicine, 2002, 346. Jg., Nr. 7, S. 476-483.
26 Chung KH, Chiou HY, Chen YH. Associations between serum homocysteine levels and anxiety and depression among children and adolescents in Taiwan. Sci Rep. 2017 Aug 21;7(1):8330.
27 Zhou SJ, Zhang LG, Chen HM, Li JY, Li R, Zhang XM, Wang N, Soares JC, Cassidy RM, Zheng Y, Ning Y, Wang SL, Chen JX, Zhang XY. Prevalence and clinical-demographic correlates of hyperhomocysteinemia in inpatients with bipolar disorder in a Han Chinese population. Psychiatry Res. 2018 Jan;259:364-369.
28 Folstein M, Liu T, Peter I, Buell J, Arsenault L, Scott T, Qiu WW. The homocysteine hypothesis of depression. Am J Psychiatry. 2007 Jun;164(6):861-7.
29 Hillemacher T, Frieling H, Muschler MA, Bleich S. Homocysteine and epigenetic DNA methylation: a biological model for depression? Am J Psychiatry. 2007 Oct
30 Mukai T, Kishi T, Matsuda Y, Iwata N.  A meta-analysis of inositol for depression and anxiety disorders. Human Psychopharmacology 2014; 29(1): 55-63
31 Swardfager W, Herrmann N, Mazereeuw et coll. Zinc in Depression: A Meta-Analysis. Biological Psychiatry, Volume 74, Issue 12 , Pages 872-878, 15 December 2013.
32 Spedding S. Vitamin D and depression: a systematic review and meta-analysis comparing studies with and without biological flaws. Nutrients. 2014 Apr 11;6(4):1501-18.
33 Akhondzadeh S, Tahmacebi-Pour N, Noorbala AA, Amini H, Fallah-Pour H, Jamshidi AH, et al. Crocus sativus L. in the treatment of mild to moderate depression: a double-blind, randomized and placebo-controlled trial. Phytother Res. 2005; 19(2): 148-51
34 Akhondzadeh , Fallah-Pour H, Afkham K, Jamshidi AH, Khalighi-Cigaroudi F.BMC Comparison of Crocus sativus L. and imipramine in the treatment of mild to moderate depression: a pilot double-blind randomized trial [ISRCTN45683816]. Complement Altern Med. 2004 Sep 2;4:12.
35 Noorbala A, Akhondzadeh S, Tahmacebi-Pour N, Jamshidi AH. Hydro-alcoholic extract of Crocus sativus L. versus fluoxetine in the treatment of mild to moderate depression: a double-blind, randomized pilot trial.J Ethnopharmacol. 2005 Feb 28;97(2):281-4. Epub 2005 Jan 6.
36 Kashani L, Raisi F, Saroukhani S, Sohrabi H, Modabbernia A, Nasehi AA, Jamshidi A, Ashrafi M, Mansouri P, Ghaeli P, Akhondzadeh S. Saffron for treatment of fluoxetine-induced sexual dysfunction in women: randomized double-blind placebo-controlled study. Hum Psychopharmacol. 2013 Jan;28(1):54-60. doi: 10.1002/hup.2282. Epub 2012 Dec 20.
37Amirhossein Modabbernia, Hamid Sohrabi, Abbas-Ali Nasehi, Firoozeh Raisi, Sepideh Saroukhani, Amirhossein Jamshidi, Mina Tabrizi, Mandana Ashrafi, Shahin Akhondzadeh, Effect of saffron on fluoxetine-induced sexual impairment in men: randomized double-blind placebo-controlled trial; Psychopharmacology, October 2012, Volume 223, Issue 4, pp 381–388
38 Jelodar G, Javid Z, Sahraian A, Jelodar S. Saffron improved depression and reduced homocysteine level in patients with major depression: A Randomized, double-blind study. Avicenna J Phytomed. 2018 Jan-Feb
39 Hausenblas H1, Heekin K, Mutchie HL, Anton S. A systematic review of randomized controlled trials examining the effectiveness of saffron (Crocus sativus L.) on psychological and behavioral outcomes. J Integr Med. 2015 Jul;13(4):231-40. doi: 10.1016/S2095-4964(15)60176-5.
40 Sanmukhani J, Satodia V, Trivedi J, Patel T, Tiwari D, Panchal B, Goel A, Tripathi CB. Efficacy and safety of curcumin in major depressive disorder: a randomized controlled trial. Phytother Res. 2014 Apr;28(4):579-85.

Warning!

This article is intended for informational purposes only and is not medical advice. It should not be used as a substitute for consulting a healthcare professional, nor for making a diagnosis or medical recommendation. While our dietary supplements are recognized for their high quality, they are not medications. They should not replace a varied, balanced diet or a healthy lifestyle.