Foleprim Iodine is a supplement which includes 

     • L-metyhlfolate – 600 mcg

     • Iodine – 200 mcg

L-metyhlfolate

Folate requires enzymatic conversion to L-methylfolate, which is the biologically active form of folic acid and can be prescribed as a prescription medical food. Recent data strongly suggest that L-methylfolate is an effective augmentation strategy for major depression at both the initial onset of symptoms and in patients with treatment-resistant depression. [1] 
L-methylfolate is the only form of folate that crosses the blood–brain barrier and is immediately available for neurotransmitter synthesis. L-methylfolate modulates the synthesis of monoamines, including serotonin, norepinephrine, and dopamine in a 2-step process. First, L-methylfolate acts as an important regulator of a critical cofactor known as tetrahydrobiopterin (BH4), which is necessary for the synthesis of neurotransmitters. The trimonoamine enzymes that require BH4 as a cofactor are tryptophanhydroxylase, the rate-limiting enzyme for 5-HT synthesis and tyrosine hydroxylase, the rate-limiting enzyme for DA and NE synthesis. Another mechanism of antidepressant activity of L-methylfolate is its role in the homocysteine cycle. It has been reported that higher CNS homocysteine levels are associated with depression, dementia, and stroke. [2] 
Studies have shown a link between folate deficiency and neuropsychiatric disorders. In particular, depressive symptoms are the most common neuropsychiatric manifestation of folate deficiency. Folate levels have been found to be inversely associated with depressive symptoms and with longer duration of depressive episodes. Depressed patients with folate deficiency showed a poorer response to standard treatment with antidepressants. Therefore, for patients with low plasma or red blood cell folate levels, folate augmentation during antidepressant treatment may improve patient outcomes. [3]
L-Methylfolate is a cofactor in the production of monoamines serotonin, dopamine, and norepinephrine, which are involved in the regulation of mood and the mechanisms of actions of antidepressants. The bioavailability of L-methylfolate is higher compared to folic acid. Moreover, up to 70% of depressed patients have a genetic variant of the methylenetetrahydrofolate reductase enzyme that compromises their ability to convert dietary folate or synthetic folic acid to L-methylfolate. L-Methylfolate supplementation may thus improve response to antidepressants that affect monoamines among depressed patients who do not respond adequately. [3] 
L -Methylfolate (7.5 and 15 mg) has been shown in retrospective and prospective studies to enhance antidepressant response. A double-blind, placebo-controlled trial of L-methylfolate among folate-deficient patients with major depressive disorder showed that adding L-methylfolate 7.5 or 15 mg to standard therapy significantly improved clinical and social recovery. [4]

Iodine

Iodine is required for thyroid hormone synthesis. Because of increased thyroid hormone production, increased renal iodine excretion, and fetal iodine requirements, dietary iodine requirements are higher in pregnancy than they are for non-pregnant women. As such, severe iodine deficiency in pregnancy can lead to maternal and fetal hypothyroidism. As adequate thyroid hormone is required for normal fetal development, iodine deficiency in pregnancy is associated with congenital anomalies, decreased intelligence, and cretinism as well as maternal and fetal goitre. Salt iodization is a simple, cheap, and effective means to ensure iodine intake, however large-scale iodization programmes have yet to be implemented in many settings, and despite major progress over the last four decades, it has been estimated that nearly 2 billion individuals worldwide remain at risk for iodine deficiency disorders. In many countries, pregnant women in particular are not receiving adequate iodine. In settings where iodized salt is not readily available, supplementation may provide needed iodine during pregnancy and lactation. [5] 
Several scientific societies, including the European Thyroid Association, the American Thyroid Association, and the Endocrine Society, currently recommend iodine supplementation for women who are pregnant, breastfeeding, or planning pregnancy, with specific formulas․ [6]
Iodine is an essential component of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3), necessary for normal growth, development, and metabolism during pregnancy, infancy and throughout life. When the physiological requirements for iodine are not met, a series of functional and developmental abnormalities occur, including thyroid function abnormalities. Severe iodine deficiency results in hypothyroidism, endemic goiter and cretinism, endemic mental retardation, decreased fertility, increased prenatal death, and infant mortality. High iodine intake may also cause disturbances in the thyroid function. [7,8] 
Historically, the implementation of salt-iodization programs worldwide has reduced the incidence of iodine deficiency, but 30% of the world’s population is still at risk. Iodine nutrition is a growing issue within industrialized countries including the U.S. as a result of declining iodine intake, in part due to changing dietary patterns and food manufacturing practices. Iodine is one of the most common nutrient deficiencies and is estimated to affect 35–45% of the world’s population. [9] In adults, severe deficiency presents as hypothyroidism, goiter, mental disability and decreased fertility. In children, goiter, intellectual/physical developmental impairment, deafness and cretinism can occur. [10] 
So, in summary Iodine supplementation improves some maternal thyroid indices and may benefit aspects of cognitive function in school-age children, even in marginally ID areas. Also, Iodine supplementation during pregnancy is related to improved maternal iodine status and/or thyroid function. [11]

References
[1] Pat Rabjohn, MD, PhD, is the Owner and Medical Director of Rabjohn Behavioral Institute, PLLC. https://doi.org/10.3928/00485713-20140403-07 
[2] Carlos Alberto Nogueira-de-Almeida, Idiberto José Zotarelli-Filho, Maria Eduarda Nogueirade- Almeida, Caio Gonçalves Souza, Vitorio Luis Kemp & Williams Santos Ramos. (2023) Neuronutrients and Central Nervous System: A Systematic Review. Central Nervous System Agents in Medicinal Chemistry
[3] Shelton RC, Sloan Manning J, Barrentine LW, Tipa EV. Assessing Effects of l-Methylfolate in Depression Management: Results of a Real-World Patient Experience Trial. Prim Care Companion CNS Disord. 2013;15(4):PCC.13m01520. doi: 10.4088/PCC.13m01520. Epub 2013 Aug 29. PMID: 24392264; PMCID: PMC3869616.
[4] Godfrey PS, Toone BK, Carney MW, et al. Enhancement of recovery from psychiatric illness by methylfolate. Lancet. 1990;336(8712)
[5] Elizabeth N. Pearce, M.D., M.Sc.Section of Endocrinology, Diabetes, and Nutrition, Boston University School of Medicine, June 2017
[6] Lopes CA, Prazeres S, Martinez-de-Oliveira J, Limbert E, Lemos MC. Iodine Supplementation in Pregnancy in an Iodine-Deficient Region: A Cross-Sectional Survey. Nutrients. 2022 Mar 27;14(7):1393. doi: 10.3390/nu14071393. PMID: 35406006; PMCID: PMC9002466.
[7] FAO/WHO. 2nd ed. Geneva: World Health Organization; 2005. Vitamin and mineral requirements in human nutrition.
[8] Nordic Nutrition Recommendations 2004. 4th ed. Denmark: Arhus; 2005. Integrating nutrition and physical activity. Nordic Council of Ministers.
[9] Hatch-McChesney A, Lieberman HR. Iodine and Iodine Deficiency: A Comprehensive Review of a Re-Emerging Issue. Nutrients. 2022 Aug 24;14(17):3474. doi: 10.3390/nu14173474. PMID: 36079737; PMCID: PMC9459956.
[10] Dunn J. Iodine. In: Shils M., editor. Modern Nutrition in Health and Disease. 10th ed. Lippincott Williams & Wilkins; New York, NY, USA: 2006.
[11] Gunnarsdottir I, Dahl L. Iodine intake in human nutrition: a systematic literature review. Food Nutr Res. 2012;56. doi: 10.3402/fnr.v56i0.19731. Epub 2012 Oct 9. PMID: 23060737; PMCID: PMC3468836.