Does Vitamin D Status Impact Sleep Quality?

Vitamin D Council

Research suggests that vitamin D may help improve common sleep disorders.

Do you have a difficult time falling and/or staying asleep, or feel restless at night and fatigued during the day? If so, you may be one of approximately 80 million Americans who struggle with a sleep disorder.

Quality sleep is crucial for supporting both mental and physical health. The science behind why sleep is so important remains elusive, but it is clear that sleep is a life-sustaining function. In fact, researchers theorize sleep is required to enable the body to repair or restore what is lost while awake.

Most of us can attest to the negative impact sleep deprivation has on our health. From memory loss and mood changes to impaired judgement and loss of physical drive, sleep disorders pose a serious threat to long-term health. In fact, when left unmanaged, sleep disorders have been linked with an increased risk in heart disease, stroke and mortality.

Research suggests that vitamin D, also known as the “sunshine vitamin,” may be a useful tool in managing two common sleep disorders, insomnia and obstructive sleep apnea.

How vitamin D may improve sleep quality:

  1. Circadian rhythm:
The circadian rhythm is our body’s internal clock that instructs us when to sleep, eat, and rest. The sun plays an important role in regulating circadian rhythms in humans, and research suggests vitamin D mediates this relationship.

This theory has been supported by several studies which have found low vitamin D status is linked with disordered sleeping habits, and that vitamin D supplementation improves sleep quality.

  1. Inflammation & muscle function:
The muscles that line the throat must work synergistically to promote regular breathing and proper swallowing. In cases of obstructive sleep apnea, these muscles intermittently relax during sleep, temporarily cutting off airway supply. The lack of oxygen reaching the tissues stimulates inflammatory pathways, and eventually results in gasping or startling awake.

Researchers theorize that vitamin D may help manage sleep apnea through its ability to reduce inflammation in the body by suppressing inflammatory pathways. In addition, vitamin D has been proven to improve muscle function.

Research on vitamin D and sleep quality:

The relationship between vitamin D and sleep has been evaluated by over 200 studies in the last 10 years, with research suggesting vitamin D deficiency is associated with more disrupted sleep and less overall sleep among a variety of populations.

One study conducted in 2012 found that maintaining vitamin D levels between 60-80 ng/ml improved sleep quality and neurological outcomes. These findings were further validated by a randomized controlled trial published in 2017 that found vitamin D supplementation helped improve sleep quality in adults who suffer from insomnia. Furthermore, a recent study found that vitamin D deficiency was associated with a lack of response to medication among insomnia patients.

Vitamin D and obstructive sleep apnea:

Research continues to grow regarding the role of vitamin D in sleep apnea, with the overarching findings suggesting vitamin D status is closely related to sleep apnea among both children and adults.

A study published in 2016 found that 98% of those with sleep apnea had low vitamin D levels (< 30 ng/ml). Another study found low vitamin D levels were linked with snoring and obstructive sleep apnea in children. Furthermore, a paper published in 2017 found low vitamin D levels was associated with increased sleep apnea severity. These findings led the Vitamin D Council to conduct a podcast with Dr. Joel Gould, Dr. Ronaldo Piovezan, and Dr. John Cannell, leading experts on this topic, to gain further insight.

Vitamin D recommendations:

The body’s sleep cycle appears to be yet another system that requires vitamin D to function properly. However, it is important to note that there are a variety of factors that impact sleep quality, so vitamin D alone may not completely resolve sleep disorders.

However, due to the safety and affordability of supplementation, the Vitamin D Council recommends adults supplement with 5,000 to 10,000 IU (125–250 mcg) vitamin D3 daily in order to reach healthy vitamin D levels (40–80 ng/ml) and thus support healthy sleeping patterns. Of course, the only way to ensure your vitamin D needs are being met, is to have your vitamin D levels tested.

If you would like to share your experience with vitamin D and sleep quality with the Vitamin D Council, or have any questions we can help answer, please email us at: info@vitamindcouncil.org. To learn more about the role of vitamin D in a variety of health outcomes, check out our website at: www.vitamindcouncil.org.

Editor’s note: Life Extension suggests maintaining an optimal range of 50–80 ng/ml in the blood. This differs from the standard reference range which is 30 ng/ml.

Citation

Sturges, M. Does vitamin D status impact sleep quality? The Vitamin D Council Blog & Newsletter, 2017.

Anti-Aging Compound Myricetin offers Heart, Brain, and Anti-Cancer Benefits

Myricetin is a naturally-occurring phenolic compound that is found in vegetables, fruits, nuts, berries, tea, and red wine. “Myricetin is a common plant-derived flavonoid and is well recognized for its nutraceuticals value,” D. K. Semwal and colleagues at South Africa’s Tshwane University of Technology remark in a recent review.

The compound exhibits a wide range of activities that include strong antioxidant, anticancer, antidiabetic and anti-inflammatory activities. It displays several activities that are beneficial for the central nervous system and numerous studies have suggested that the compound may be beneficial to protect against diseases such as Parkinson's and Alzheimer's.”1 In an evaluation of compounds derived from the plant Triclisia gilletii, myricetin showed activity against a resistant strain of Mycobacterium tuberculosis.2 In another study, myricetin and glycosylated metabolites of myricetin inhibited human immunodeficiency virus (HIV) type 1.3

Cardiovascular Research on Myricetin

An investigation of eight plant compounds found that myricetin protected human vascular endothelial cells from hydrogen peroxide-induced oxidative injury and lowered the formation of thiobarbituric acid reactive substances (TBARS, a marker of lipid peroxidation).4 “Taken all together the results indicate myricetin as the most active agent among the selected plant-derived polyhydroxyl compounds, with prominent capacities against oxidized LDL and reactive oxygen species production in human umbilical vascular endothelial cells,” R. Bertin and colleagues conclude.

In the heart, myricetin reduced the ability of the proinflammatory compound lipopolysaccharide to cause injury in a mouse model of sepsis-induced myocardial dysfunction.5 The compound decreased the production of inflammatory cytokines in heart tissue and serum while reducing apoptosis (programmed cell death), thereby preventing the impairment in cardiac function that was observed in animals that did not receive myricetin.

In experiments involving skin cells known as keratinocytes, and also fibroblasts and endothelial cells, myricetin-3-O-beta-rhamnoside and the phenolic compound chlorogenic acid exhibited wound healing properties.6 Myricetin has also been found to protect against ultraviolet-B damage in human keratinocytes.7

Research in mice in which diabetes was induced by the administration of streptozotocin revealed that six months of treatment with myricetin reduced cardiac hypertrophy, apoptosis, and interstitial fibrosis.8 Myricetin was found to strengthen antioxidative activity and decrease the production of malondialdehyde, a marker of oxidative stress, while lowering the secretion of the inflammatory cytokines interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha. The authors concluded that myricetin possesses potential protective effects against diabetic cardiomyopathy, which is associated with an increased risk of premature mortality in diabetics.

Myricetin, Brain, and Cognitive Function

Research has revealed that myricetin can reduce some of the consequences of the genetic abnormalities in Huntington’s disease while improving neurobehavioral deficits in a mouse model.9 The research suggests that myricetin could be investigated as a treatment for Huntington’s disease and related disorders.

In a mouse model of Alzheimer’s disease, myricetin reversed cognitive deficits by inhibiting acetylcholinesterase (the enzyme that breaks down the neurotransmitter acetylcholine), and by downregulating brain iron.10 Myricetin lowered oxidative damage and increased antioxidant enzyme activity, an effect that was prevented by a high iron diet.

In a study involving mice in which cognitive impairment was induced by the administration of D-galactose, myricetin significantly improved memory and learning.11 Myricetin has demonstrated the ability to protect against glutamate-induced excitotoxicity, and the authors concluded that “myricetin is a potent antineurodegenerative compound and may contribute to the discovery of a drug with which to combat neurodegeneration.”12

Myricetin and Cancer

A review of natural compounds used in the treatment of non-small cell lung cancer included information concerning the benefit of myricetin.13 “Myricetin, a flavonoid commonly found in tea, wines, berries, fruits, and medicinal plants, has been reported to possess antioxidative, antiproliferative, and anti-inflammatory qualities,” Chih-Yang Huang and colleagues write. “Previous studies have shown that myricetin exerts an antiproliferative effect on lung, esophageal, leukemia, and prostate cancer cells. Myricetin may act as a direct antioxidant that scavenges or quenches oxygen free radicals, and as an indirect antioxidant that induces antioxidant enzymes to protect cells against hydrogen peroxide-induced cell damage.”

Myricetin’s anti-inflammatory effect showed an ability to prevent chronic inflammation and decreased the size of colon polyps, a precursor of colorectal cancer in mice.14 The compound lowered levels of the inflammatory factors interleukin-1beta, interleukin-6, tumor necrosis factor-alpha, nuclear factor NF-κB, cyclooxygenase-2 (COX-2), and other factors in colon tissues. The findings suggest its use “as a promising chemopreventive drug for reducing the risk of colorectal cancer”, according to authors M. J. Zhang and colleagues.

In oral squamous cell carcinoma cells, myricetin impaired cell cycle progression and inhibited metastasis.15 In placental choriocarcinoma (a cancer that affects pregnant women) cells, myricetin decreased cell proliferation and promoted apoptosis.16 It also showed synergistic effects with the chemotherapies etoposide and cisplatin. In anaplastic thyroid cancer (an often lethal form of thyroid cancer) cells, myricetin reduced proliferation by about 70%.17 In human glioma (a cancer of the brain and spinal cord) cells, myricetin inhibited cell migration, induced apoptosis and elicited other anticancer effects.18 The compound has shown an ability to induce apoptosis and other effects in human ovarian, esophageal, colon, prostate, bladder, pancreatic, liver, and stomach cancer cells.19-26

Myricetin has additionally shown an ability to enhance natural killer cell activity, which can increase the ability to combat cancer.27

“An increasing number of studies have shown the beneficial effects of myricetin against different types of cancer by modifying several cancer hallmarks including aberrant cell proliferation, signaling pathways, apoptosis, angiogenesis, and tumor metastasis,” writes K. P. Devi and colleagues in a 2015 review. “Most importantly, myricetin interacts with oncoproteins such as protein kinase B (PKB) (Akt), Fyn, MEK1, and JAK1-STAT3 (Janus kinase-signal transducer and activator of transcription 3), and it attenuates the neoplastic transformation of cancer cells. In addition, myricetin exerts antimitotic effects by targeting the overexpression of cyclin-dependent kinase 1 (CDK1) in liver cancer.”28

Lifespan and Anti-aging Effects

In regard to myricetin’s potential benefits, here's the best part: research has found that the compound extended average lifespan by 32.9% when administered to the roundworm Caenorhabditis elegans.29 Longer life was accompanied by a decline in reactive oxygen species accumulation and less formation of lipofuscin which is “a pigment consisting of highly oxidized and cross-linked proteins that is considered as a biomarker of aging in diverse species.” However, the authors conclude that, rather than its direct antioxidant effects, myricetin’s lifespan-extending benefit is dependent on the transcription factors DAF-16.

On the research horizon, the structure of myricetin helped in the development of a new compound (Proxison) that has even greater antioxidant potency.30 “This novel antioxidant can be applied to investigate oxidative stress in disease models, like alpha-synucleinopathies and other neurodegeneration models,” Nicola J. Drummond and colleagues conclude. “In addition, Proxison could have applications for regenerative medicine where oxidative stress has been implicated in poor cell survival of transplanted cells, with the advantage that the molecule can be pre-loaded into cells prior to transplantation. Proxison could also have applications for conditions, such as stroke or cardiac infarction, in which a temporary, but acute, exposure to oxidative stress is experienced, as well as diseases in which oxidative stress and mitochondrial dysfunction are core features.”

Furthermore, myricetin was recently identified as one of a handful of compounds that modify senescence-inducing pathways.31 This and other research suggests its use by humans to help decelerate aging. It will be of benefit to all life extensionists to keep up-to-date concerning the outcome of future research involving this promising flavonoid.

References

  1. Semwal DK et al. Nutrients. 2016 Feb 16;8(2):90.
  2. Tiam ER et al. Nat Prod Res. 2017 Nov 16:1-9.
  3. Ortega JT et al. AIDS Res Ther. 2017 Oct 12;14(1):57.
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  5. Zhang N et al. Phytother Res. 2017 Dec 7.
  6. Moghadam SE et al. Molecules. 2017 Sep 8;22(9).
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  8. Liao HH et al. Oxid Med Cell Longev. 2017;2017:8370593.
  9. Khan E et al. ACS Chem Biol. 2017 Nov 27.
  10. Wang B et al. Biochem Biophys Res Commun. 2017 Aug 19;490(2):336-342.
  11. Lei Y et al. Food Chem. 2012 Dec 15;135(4):2702-7.
  12. Shimmyo Y et al. J Neurosci Res. 2008 Jun;86(8):1836-45.
  13. Huang CY et al. Biomedicine (Taipei). 2017 Dec;7(4):23.
  14. Zhang MJ et al. Biomed Pharmacother. 2017 Nov 9;97:1131-1137.
  15. Maggioni D et al. Nutr Cancer. 2014;66(7):1257-67.
  16. Yang C et al. Cancer Lett. 2017 Jul 28;399:10-19.
  17. Jo S et al. Anticancer Res. 2017 Apr;37(4):1705-1710.
  18. Li HG et al. J BUON. 2016 Jan-Feb;21(1):182-90.
  19. Xu Y et al. Mol Med Rep. 2016 Mar;13(3):2094-100.
  20. Zang W et al. Tumour Biol. 2014 Dec;35(12):12583-92.
  21. Kim ME et al. Anticancer Res. 2014 Feb;34(2):701-6.
  22. Xu R et al. Food Chem. 2013 May 1;138(1):48-53.
  23. Sun F et al. Nutr Cancer. 2012;64(4):599-606.
  24. Phillips PA et al. Cancer Lett. 2011 Sep 28;308(2):181-8.
  25. Zhang X et al. Zhongguo Zhong Yao Za Zhi. 2010 Apr;35(8):1046-50.
  26. Feng J et al. Mol Cell Biochem. 2015 Oct;408(1-2):163-70.
  27. Lindqvist C et al. Anticancer Res. 2014 Aug;34(8):3975-9.
  28. Devi KP et al. Life Sci. 2015 Dec 1;142:19-25.
  29. Büchter C et al. Int J Mol Sci. 2013 Jun 4;14(6):11895-914.
  30. Drummond NJ et al. Sci Rep. 2017 Sep 19;7(1):11857.
  31. Kreshin S. Life Extension. 2017 Apr.

Allantoin: The Vitamin-Like Compound for Skin and Anti-Aging Benefits

Allantoin is a compound that occurs in aloe vera, chamomile, lotus, yam, and other plants.

Allantoin can also be chemically synthesized. Within the body, it acts as a free radical scavenger. 1



Allantoin Activity is Similar to a Vitamin

In an article published in 2004, E. P. Gus'kov and colleagues suggest that allantoin acts as a vitamin.

“Inactivation of the gene Uox in primates, which is responsible for the synthesis of the enzyme uricase, has determined new ways of social and intellectual evolution of mammals,” they observed. “Almost simultaneously with this process, a mutation occurred, as a result of which primates lacked the capability of endogenous synthesis of ascorbate. These mutations sharply changed the systems of antioxidant defense by eliminating vitamin C and allantoin from the overall profile of intracellular nonenzymatic inactivation of reactive oxygen species.”2

The authors discuss the ways in which allantoin behaves like a water-soluble vitamin. They note that in water solutions, the antioxidative properties of allantoin and ascorbic acid are similar, suggesting that allantoin could be regarded as a vitamin.

Allantoin, Wound Healing, and Skin Health

Research has revealed a benefit for allantoin in wound healing.3 When combined with other compounds, it has been shown to help prevent intra-abdominal adhesions after surgery and reduce redness and the formation of new blood vessels in hypertrophic scars and keloids, which was associated with improvement in skin lesions.4,5

“Allantoin, 5-ureide-hydantoin, has been widely cited in literature as holder of numerous pharmacological activities, among them: wound healing, anti-irritating, hydrating and remover of necrotic tissue, stimulating the cell mitosis; as well as promoter of epithelial stimulation, analgesic action and keratolytic activity,” observe researchers Lorena Ulhôa Araújo and colleagues in a recent article. “For all these reports, allantoin has been used in cosmetic and pharmaceutical preparations for over 70 years with different therapeutic purposes and especially as a wound healing booster.”6

The results of research reported by Araújo and her associates suggests that the wound healing mechanisms induced by allantoin include regulation of the inflammatory response and stimulation of fibroblast proliferation and extracellular matrix synthesis.6 In addition to lowering inflammation, research has shown an ability for allantoin to relieve pain that involves the opioid receptor.7

In addition to healing the skin, allantoin has shown promise against asthma in a mouse model.8 Animals treated with allantoin had lower levels of immunoglobulin E and cytokines that included interleukins 4 and 5 in bronchoalveolar lavage fluid, as well as less inflammatory cell infiltration compared to a control group. The effectiveness of the compound was similar to that of the asthma and allergy drug montelukast.

Blood Sugar and Beyond

In diabetic rats, allantoin dose-dependently decreased plasma glucose.9 Treated animals also experienced an increase in plasma beta-endorphin, a hormone used by the body in the reduction of stress. Allantoin additionally enhanced beta-endorphin release from adrenal glands isolated from diabetic rats. Further investigation demonstrated that allantoin increased glucose uptake in skeletal muscle.

Research has determined that allantoin can activate imidazoline receptors that are also activated by the drug metformin to lower blood sugar. It has been noted that allantoin has a chemical structure similar to metformin.10

In a study involving insulin-producing pancreatic beta cells treated with the diabetes-inducing compound streptozotocin, allantoin limited apoptosis (programmed cell death) and cell toxicity and increased the cells’ viability.11 When injected into streptozotocin-treated rats, allantoin lowered plasma glucose levels. M. Amitani and colleagues concluded that “allantoin and related analogs may be effective in the therapy for beta-cell damage.”

In another study involving rats rendered diabetic by streptozotocin injection, one-month treatment with allantoin lowered glucose, hemoglobin A1c, total cholesterol, low-density lipoprotein (LDL) cholesterol, and malondialdehyde (a marker of lipid peroxidation) compared to animals that received streptozotocin alone.12 Additionally, improvements were observed in levels of the antioxidant enzyme superoxide dismutase, glutathione, and other factors. The administration of crude yam (Dioscorea batatas) powder and a water extract of yam, both of which contain allantoin, were also associated with improvements. Yam peel has also been shown to contain a high amount of allantoin, which may have antioxidant and antitumor effects.13

The Anti-Aging Effects of Allantoin

Allantoin has shown memory-enhancing effects while increasing the proliferation of immature neurons in the hippocampal dentate gyrus region in the brains of mice, which suggested to the scientists involved in the research “that allantoin has therapeutic potential for the cognitive dysfunctions observed in Alzheimer's disease.”14

Allantoin has been recently identified as a mimetic of calorie restriction.15 Caenorhabditis elegans worms that received allantoin lived 20% longer than untreated worms and differently expressed several hundred genes. “We have shown that rapamycin, LY‐294002, TSA and allantoin can increase lifespan in C. elegans in a manner that does not act synergistically with calorie restriction‐induced lifespan extension, indicating that these compounds and calorie restriction may act through a similar mechanism,” write S. Calvert and colleagues. “Additionally, we have shown that this lifespan extension comes with a possible slowing of aging seen through a moderately slower decline in pharyngeal pumping rate, but with no change in movement rate decline.”

They add that allantoin has been found to bind to imidazoline receptors and have beneficial effects on energy regulation, possibly through the activation of AMP kinase which could then act through the mTOR (mechanistic target of rapamycin) pathway.

A subsequent study involving the identification of mimetics of the healthspan-extending drugs metformin and rapamycin via bioinformatic approaches and deep learning methods identified allantoin as a metformin mimetic.16 “The compound exhibiting the highest similarity to metformin according to the metformin classifier was allantoin, a key beneficial compound in yam (Dioscorea spp.),” A. Aliper and colleagues write. “Being a guanidinium derivative, allantoin is similar to metformin in structure and has been shown to induce glucose lowering effects via imidazoline I-2 receptors.” However, more safety data is required to support the use of orally administered allantoin.

While metformin is a prescription drug and allantoin is not available as a supplement, you can obtain some of the plant sources of the compound and find topical products that contain it. Research has determined that allantoin and allantoin complexes are safe at commonly used concentrations.17

References

  1. Gus'kov EP et al. Dokl Biochem Biophys. 2002 Mar-Apr;383:105-7.
  2. Gus'kov EP et al. Dokl Biochem Biophys. 2004 Sep-Oct;398:320-4.
  3. Klouchek-Popova E et al. Acta Physiol Pharmacol Bulg. 1982;8(4):63-7.
  4. Wang XC et al. World J Gastroenterol. 2003 Mar;9(3):568-71.
  5. Campanati A et al. Dermatol Surg. 2010 Sep;36(9):1439-44.
  6. Araújo LU et al. Acta Cir Bras. 2010 Oct;25(5):460-6.
  7. Florentino IF et al. J Ethnopharmacol. 2016 Jun 20;186:298-304.
  8. Lee MY et al. Int Immunopharmacol. 2010 Apr;10(4):474-80.
  9. Niu CS et al. J Agric Food Chem. 2010 Nov 24;58(22):12031-5.
  10. Lin KC et al. Horm Metab Res. 2012 Jan;44(1):41-6.
  11. Amitani M et al. PeerJ. 2015 Aug 6;3:e1105.
  12. Go HK et al. Nutrients. 2015 Oct 15;7(10):8532-44.
  13. Liu Y et al. J Food Sci. 2016 Jun;81(6):H1553-64.
  14. Ahn YJ et al. Food Chem Toxicol. 2014 Feb;64:210-6.
  15. Calvert S et al. Aging Cell. 2016 Apr;15(2):256-66.
  16. Aliper A et al. Aging (Albany NY). 2017 Nov 15;9(11):2245-2268.
  17. Becker LC et al. Int J Toxicol. 2010 May;29(3 Suppl):84S-97S.

Brain Food: Keep Your Eyes on Spinach

Spinach (Spinacia oleracea) is a leafy green vegetable that is a member of the Amaranthaceae, or amaranth family. This family of flowering plants derives its name from a Greek word that means “unfading,” or “unwilting,” and is symbolic of immortality.

Popeye had a point. Spinach may not grow muscle, but its healthy properties make the body strong in other ways.

The Biological Activity of Spinach

A current review of the functional properties of spinach notes that, “Spinach-derived phytochemicals and bioactives are able to (i) scavenge reactive oxygen species and prevent macromolecular oxidative damage, (ii) modulate expression and activity of genes involved in metabolism, proliferation, inflammation, and antioxidant defense, and (iii) curb food intake by inducing secretion of satiety hormones. These biological activities contribute to the anticancer, antiobesity, hypoglycemic, and hypolipidemic properties of spinach. Despite these valuable attributes, spinach consumption remains low in comparison to other leafy green vegetables.”1

Nutrients Found in Spinach

Spinach is a good source of beta-carotene, vitamin C, vitamin K, magnesium, folate, manganese, calcium, potassium and fiber. It contains a significant amount of iron; however, its high oxalate content can bind to the mineral, rendering it unabsorbable. Spinach has gained the spotlight recently as a source of lutein and zeaxanthin. These carotenoids accumulate in the macula of the eye, where they are known as macular pigment.

Spinach for Eye and Brain Health

Increased intake of lutein and zeaxanthin help protect against age-related macular degeneration, a common source of vision loss. Not only is lutein helpful to the eyes, but a recent study also found an association between higher serum lutein levels and so-called crystallized intelligence: the ability to retrieve and use information acquired throughout life.2 Men and women enrolled in the study who had higher lutein levels also had thicker gray matter in the parahippocampal cortex of the brain, leading co-lead researcher Aron Barvey to conclude that "Gray-matter volume of the parahippocampal cortex on the right side of the brain accounts for the relationship between lutein and crystallized intelligence."

In a study reported in the Journal of the International Neuropsychological Society,higher lutein and zeaxanthin levels were associated with more efficient brain activity in older adults.3 "There's a natural deterioration process that occurs in the brain as people age, but the brain is great at compensating for that,” explained first author Cutter Lindbergh, of the University of Georgia. “One way it compensates is by calling on more brain power to get a job done so it can maintain the same level of cognitive performance."

"It's in the interest of society to look at ways to buffer these decline processes to prolong functional independence in older adults," he noted. "Changing diets or adding supplements to increase lutein and zeaxanthin levels might be one strategy to help with that."

A recent review suggests a role for spinach in the prevention of Alzheimer’s disease.4 Spinach’s ability to improve cognition, act as a source of antioxidant polyphenolic compounds, help protect against amyloid beta toxicity and inhibit the breakdown of acetylcholine could all help protect against the development of the disease or slow its progression.

Other Health Benefits of Spinach

In mice given a high fat, high fructose diet, nitrate-enriched spinach improved lipids, lowered insulin resistance and inflammation (as indicated by a reduction in serum C-reactive protein, tumor necrosis factor alpha and interleukin-6), and improved vascular endothelial function.5 Research has also uncovered a protective role for lutein and zeaxanthin against nonalcoholic fatty liver disease (NAFLD).6

In a rat model of menopausal osteopenia, spinach extract prevented bone loss in tandem with an increase in the expression of osteogenic genes.7 In animals that underwent induced fractures, bone regeneration was accelerated in association with the intake of dried spinach extract.

In a study in which 8 human subjects consumed 225 grams per day of spinach over a 16-day period, oxidative damage to DNA in lymphocytes (a type of white blood cell) was lowered while folate levels increased and homocysteine levels were reduced.8

There is evidence that spinach has an anticancer effect. A glycolipid fraction of spinach given for two weeks to mice that received colon adenocarcinoma tumor grafts resulted in a 56.1% decrease in solid tumor volume without side effects.9 Mechanisms identified include inhibition of angiogenesis (new blood vessel formation) in tumor tissue and a decrease in cell proliferation. Spinach glycolipid fraction has also shown an inhibitory effect against human cervical cancer in mice that received implanted tumors.10 In human prostate cancer cells, antioxidants derived from spinach, particularly NAO, inhibited cellular proliferation while decreasing reactive oxygen species.11 And in human gastric adenocarcinoma cells, powdered spinach extract inhibited cell proliferation and viability, as well as DNA synthesis.12

Fresh spinach sautéed with garlic in olive oil is delicious as a side dish. The leaves can be added to salads, blended with other vegetables or fruit in smoothies or chopped and added to pasta. However, if you truly don’t like spinach, you can now obtain some of its unique benefits in the form of lutein/zeaxanthin supplements, alone or in many eye support formulas.

References

  1. Roberts JL et al. Food Funct. 2016 Aug 10;7(8):3337-53.
  2. Zamroziewicz MK et al. Front Aging Neurosci. 2016 Dec 6;8:297.
  3. Lindbergh CA et al. J Int Neuropsychol Soc. 2017 Jan;23(1):11-22.
  4. Jiraungkoorskul W. Pharmacogn Rev. 2016 Jul-Dec;10(20):105-108.
  5. Li T et al. Food Nutr Res. 2016 Sep 9;60:32010.
  6. Murillo AG et al. Biology (Basel). 2016 Nov 8;5(4).
  7. Adhikary S et al. Menopause. 2017 Jan 23.
  8. Moser B et al. Eur J Nutr. 2011 Oct;50(7):587-94.
  9. Maeda N et al. Lipids. 2008 Aug;43(8):741-8.
  10. Maeda N et al. Nutr Cancer. 2007;57(2):216-23.
  11. Nyska A et al. Toxicol Pathol. 2003 Jan-Feb;31(1):39-51.
  12. He T et al. Biomed Environ Sci. 1999 Dec;12(4):247-52.

Diet and Supplement Options for Kidney Disease

The kidneys consist of two organs situated on either side of the body, below the ribs. Among other functions, the kidneys filter the blood, a function that is vital to life. Kidney disease occurs when the organs’ ability to filter wastes from the blood becomes impaired, leading to an elevation of harmful compounds. Kidney failure is sometimes diagnosed as acute, which requires immediate intensive treatment and is usually reversible. Chronic renal failure (CRF), on the other hand, can develop over time and, in the absence of a kidney transplant, requires a lifetime of treatment. Other than dialysis or a transplant, can anything be done for kidney disease?

Supplements

A study reported in Diabetes Care demonstrated improvement in the kidney function of type 1 diabetics who received orally administered vitamin E, as indicated by normalization of the kidneys’ ability to clear the waste product creatinine.1 Elevated creatinine is a hallmark of kidney disease.

B-Vitamins

In diabetic rats, thiamine and benfotiamine (forms of vitamin B1) inhibited the development of microalbuminuria (increased albumin in the urine, another indicator of diseased kidneys) by 70%–80% in comparison with animals that did not receive the vitamin.2 Authors R. Babaei-Jadidi and colleagues proposed that, “Clinical diabetic subjects should avoid becoming thiamine deficient, even weakly so, and that high-dose thiamine repletion should be considered for therapy to prevent the development of clinical diabetic nephropathy.”

Vitamin B6 may also play a protective role in the kidneys. In a double-blind trial, researchers assigned 317 diabetics who had protein in their urine to receive a placebo or one of two doses of the vitamin B6 derivative pyridoxamine dihydrochloride twice per day for a year.3 Among participants whose initial serum creatinine levels were among the lowest third (which indicates less advanced kidney dysfunction), treatment with the higher dose of pyridoxamine hydrochloride was associated with half the rise in creatinine levels over the course of the study in comparison with the placebo, which suggests that the compound could slow the progression of less advanced disease.

Another B vitamin, folic acid, was shown to delay the progression of chronic kidney disease in hypertensive men and women treated with the blood pressure drug enalapril.4 Among subjects who had chronic kidney disease at the beginning of the study, the risk of experiencing specific decreases in the kidney’s estimated glomerular filtration rate was significantly less among subjects who received folic acid plus enalapril than among those who received enalapril alone. "Our study is the first to show significant renal protection from folic acid therapy in a population without folic acid fortification," Xin Xu, MD, PhD, and colleagues announce." Given the magnitude of renal protection suggested by this study as well as the safety and the low cost, the potential role of folic acid therapy in the clinical management of patients with chronic kidney disease in regions without folic acid fortification should be vigorously examined."

Vitamin D

African Americans are disproportionally affected by kidney failure. A study published in 2009 in the Journal of the American Society of Nephrology found a significant association between end stage renal disease (ESRD) and insufficient vitamin D levels in African American subjects.5 According to lead author Michal L. Melamed, MD, "We found that 25-hydroxyvitamin D deficiency was responsible for about 58 percent of the excess risk for ESRD experienced by African Americans."

Other research concluded that vitamin D deficiency is nearly universal among patients with reduced albumin levels who started hemodialysis during winter, when vitamin D levels may be lower.6 And in a study of patients with the autoimmune disease systemic lupus erythematosus (SLE), those with abnormally low vitamin D levels had an 87% greater risk of kidney damage than those whose levels of the vitamin were sufficient.7 "Supplementing vitamin D reduces urine protein, which is the best predictor of future renal failure," commented researcher Michelle Petri, MD, PhD, of the Johns Hopkins University Lupus Center. "Supplementary vitamin D is very safe. It helps to prevent one of the most dreaded complications of SLE, and likely has a role in preventing blood clots and cardiovascular disease as well. Vitamin D supplementation, which can reduce proteinuria, should be a part of the treatment plan for lupus nephritis patients."

Diet

In a randomized trial that included 101 chronic kidney disease patients, those who received pomegranate juice prior to hemodialysis sessions had less oxidative stress, inflammation, lower risks of hospitalization due to infection, and atherosclerosis progression after one year compared to participants who received a placebo.8 "Considering the expected epidemic of chronic kidney disease in the next decade, further clinical trials using pomegranate juice aimed at reducing the high cardiovascular morbidity of chronic kidney disease patients and their deterioration to end-stage renal disease should be conducted," recommended lead researcher Bayta Kristal, MD, of Technicon-Israel Institute of Technology.

To lower the risk of developing kidney disease in the first place, a Mediterranean diet, which is high in plant foods, fish and healthy fats, could help.9 Researchers at Columbia University determined that for each one-point increase in Mediterranean diet score (indicating greater adherence to the diet) there was a 17% reduction in the risk of developing chronic kidney disease, and among those whose scores were indicative of the closest adherence to the diet, a 50% lower risk of developing the disease was observed.

For patients with chronic renal failure, physicians typically prescribe a diet that contains limited amounts of fluids, protein, sodium, potassium and phosphorous. The results of a number of studies indicate that specific nutritional supplements may also be helpful. If you have kidney disease and are considering supplementation with any of these nutrients, it is essential to discuss with your physician whether any of these nutrients can be safely used, and to inform him/her of any changes in your supplement regimen.

References


  1. Bursell SE et al. Diabetes Care. 1999 Aug;22(8):1245-51.
  2. Babaei-Jadidi R et al. Diabetes. 2003 Aug;52(8):2110-20.
  3. Lewis EJ et al. J Am Soc Nephrol. 2012 Jan;23(1):131-6.
  4. Xu X et al. JAMA Intern Med. 2016 Oct 1;176(10):1443-1450. 2017.
  5. Melamed ML et al. J Am Soc Nephrol. 2009 Dec;20(12):2631-9.
  6. Bhan I et al. Clin J Am Soc Nephrol. 2010 Mar;5(3):460-7.
  7. Petri M et al. American College of Rheumatology/Association of Rheumatology Health Professionals (ACR/ARHP) Annual Meeting. 2017 Nov 5.
  8. Shema-Didi L et al. Free Radic Biol Med. 2012 Jul 15;53(2):297-304.
  9. Khatri M et al. Clin J Am Soc Nephrol. 2014 Nov 7;9(11):1868-75.

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