With that in mind let’s see how to identify your negativity levels:
Cash do not flow easily, unpaid bills start to pile and you do not know where your money is going. Getting a stagnation in our prosperity is a sign that the path to growth is blocked even when we are earning enough money.
You feel tired, exhausted and you get frustrated easily. You experience up and downs like a rollercoaster and you feel bad about yourself. Usually, we still feel exhausted after a good’s night rest and …with a balanced diet.
You feel stressed and unable to cope with every day activities, while before everything was fine.
You are more prone to infections than normal and you start getting sick more often. Signs of a low immune system topped up with stress.
Communication is affected, people seem to not being able to understand you and you feel that you don’t understand others.
You find difficult to care for yourself and you cannot find any time for yourself.
Your sleep pattern is affected with strange dreams and nightmares. Your subconscious mind tries to alert you that something is not right.
Negative thoughts and emotions seem to surface every time you are trying to relax. What is worse is that the more you try to stop them the more resistant they become.
Losing keys, money, wallets, clothes etc and having a difficult time to find them, even though most of the time they are around you and quite visible.
Feel unable to concentrate as your mind tends to focus on random things while you experience a feeling of emptiness.
Ok if you experience more than 5 of these together then it is time to make a change –
If you are in that conspiracy theory frequency, you NEED to get out of that vibration, which is a fear based vibration. “Energy flows where your attention goes.” and what you put your attention on is just going to increase and accelerate as time goes on. Get as far away from that shit as you can LOL!!!!! Stop giving ur power away.
MOST IMPORTANTLY YOU MUST!!!! REPROGRAM YOUR SUBCONSCIOUS MIND!
ALSO CONNEC TO THE REALITY/VERSION OF UR SELF YOU WANT TO LIVE AS!
MOST IMPORTANTLY YOU MUST!!!! REPROGRAM YOUR SUBCONSCIOUS MIND!
SO CONNECt TO THE REALITY/VERSION OF UR SELF That YOU WANT TO LIVE AS!
Preview How to make stress your friend | Kelly McGonigal
.–Conclusions and Perspectives
The imbalance in Hcy metabolism is linked with a number of human pathologies.
It remains unclear whether excessive Hcy concentration directly contributes to the pathogenesis of diseases or it represents a biomarker of metabolic aberrations, such as aberrant methyl group metabolism. Different strategies to reduce plasma Hcy concentrations have reached inconsistent results, not just in the case of vascular disorders, but also with respect to neurodegenerative disorders, bone tissue health or cancer. hHcy leads to increased thiolation and homocysteinylation of proteins, both in plasma and in tissues.
As a consequence, these post-translational modifications affect the function and activity of different enzymes, like superoxide dismutase, catalase or glutathione peroxidase [34]. Aberrant Hcy metabolism leads to redox imbalance and to increased oxidative stress and formation of reactive oxygen and nitrogen species, followed by the protein, nucleic acid and carbohydrate oxidation, and lipoperoxidation.
Moreover, Hcy treatment of cell cultures doubles the rate of telomere shortening.
Elevated levels of Hcy can result from the deficiency of one or more enzyme’s vitamin cofactor involved in its metabolism. Therefore, it would be very important to find the strategies to decrease Hcy levels. It was proven that vegan or vegetarian individuals have deficiency in some vitamins, especially B6 and B12 that are involved in remethylation pathway of Hcy. These persons are more sensitive to develop hHcy [105].
Genetic abnormalities and nutritional deficiencies explain only a part of hHcy pathologies. Hormonal and metabolic factors such as diabetes, thyroid diseases and estrogen deficiency interact with Hcy metabolism [106]. In addition, therapy with multiple vitamins and folate might be as a one clue to correct Hcy level in patients. Clinical trials are needed to determine the optimal doses of vitamins.
Neural cells are sensitive to prolonged hHcy treatment, because Hcy cannot be metabolized by transsulfuration pathway or by folate/vitamin B12 independent remethylation pathway. Therefore, Hcy might be used as an additional valuable prognostic and predictive biomarker in neurodegenerative diseases.
Elevated level of Hcy detected in cancer patient is one of the major consequences of the rapid tumor cell proliferation. Potentially, circulating Hcy could be used as one of markers to monitor cancer patients during drug therapy, complementing the currently used tumor markers. More studies including larger populations are needed to verify these points and also to find an appropriate cut-off value of Hcy for patients with cancer.
Rapid proliferated tumor cells would deplete folate followed by inactivation of “one-carbon” metabolism. Their disability to convert Hcy to Met leads to increased levels of Hcy. This could be one of explanation of “methionine-dependency”of malignant cells. Refsum et al. [107] found elevated Hcy levels in children with acute lymphoblastic leukemia before beginning of drug treatment. It fell dramatically down after few days of cytotoxic drug administration.
Potentially, elevated Hcy could be a marker for carcinogenesis and also for detecting recurrence. Sun et al. [102] monitored the Hcy concentrations within the concentrations of the dominant tumor markers in a group of patients with carcinomas, who were not taking drugs. The changes of serum Hcy concentrations parallel the rise and fall with serum tumor markers.
These results suggest that serum Hcy, like tumor markers, reflected the tumor cell activity. However, Ozkan et al. [108] observed higher prevalence of hHcy in lung cancer patients is not sufficient to accept Hcy as a cancer marker. Also the Determination of Hcy in larger cancer population. . . . could be important to clarify the usefulness of Hcy as a marker for cancer and its drug therapy.
The epigenetic mechanisms play an important role in elevated Hcy production.
Since SAM is a universal donor of methyl group, SAH followed by Hcy are produced during these processes. It becomes more and more evident, that DNA methylation impairment might be suggested as consequence of hHcy caused by endogenous (polymorphisms of genes which code enzymes involved in Hcy and folate pathways) and/or exogenous factors (dietary deficiency of folate and vitamins, protein intake rich in Met and Cys) and may be involved in etiopathogenesis of Hcy toxicity.
It is important to find factors that can affect the methyl balance to help us to understand the pathophysiology of diseases from “methylation point of view”. Epigenetic alternations in mitochondrial DNA need to be evaluated in terms of prediction of therapeutic efficacy similar to nuclear DNA [109]. Advanced studies are needed to understand whether and how changes in mitochondrial DNA methylation patterns, global and gene specific are associated to elevated levels of Hcy in context to diseases and risk factors, such oxidative stress, aging and exposure to drugs.
As shown by recent studies, some natural compounds which are able to decrease the plasma level of the Hcy. Resveratrol is a polyphenol compound found in the skin of red grapes, in peanuts and berries. This plant antioxidant can protect the body against damages linked to the increased risk for cardiovascular and neurological diseases or cancer. Resveratrol strongly, but not completely, reduced platelet apoptosis induced by Hcy or Hcy-TL [110].
Another compound, paraoxonase 1 (PON1, EC 3.1.8.1) is a calcium-dependent enzyme synthesized in liver. It is a major component of plasma HDL particles, responsible for the antioxidant protection of HDL or LDL particles. PON1 hydrolyzes Hcy-TL, which is determinant of plasma N-homocysteinylated protein concentration [111]. The lactonase (Hcy-thiolactonase) activity of PON1 can help to avoid the post-translational modification of LDL apoproteins through N-homocysteinylation in HDL particles. It was confirmed, that another compound, tetrahydrocurcumin which is a herbal antioxidant, improves homocysteinylated cytochrome c mediated autophagy in hHcy mice after cerebral ischemia [112]. Tetrahydrocurcumin may be an effective protective agent in the prevention of oxidative stress induced by hHcy.
In conclusion, the increased prevalence of hHcy in the population and crucial role of elevated Hcy levels in pathogenesis of different diseases make this amino acid an interesting target for future investigations. Advanced studies are needed to understand: (i) the role of new preventative dietary supplements or medicaments, which will decrease plasma Hcy level; (ii) the molecular basis to find the mechanism of Hcy interaction with its target molecules inside the cell also in extracellular space; (iii) the epigenetic alteration of DNA (nuclear and mitochondrial) methylation profiles in correlation with pathogenesis of diseases; and (iv) usefulness and validity of Hcy as a biomarker of multimarker panel to predict (along with other factors such as age, gender, smoking, and some other genetic variants) the risk of developing and/or progression of some diseases.
First, using the methylation and detox profile features on this site require a 23andMe test. 23andMe saves close hundreds of thousands of pieces (called SNPs) of genetic data from your DNA. The test is easy, and there is no doctor needed. Just go to 23andMe.com, order a kit, spit in a tube, and they run your DNA through their lab. 23andMe has sequenced close to a million people and provides comprehensives ancestry reports and genetic health information.
23andMe provides you full access to your data. This means that when you order your kit, you will be able to use Genetic Genie for methylation and detox profiles. http://geneticgenie.org/
Beyond methylation support, what can we do to mitigate the effects of too much homocysteine? While you’re working on bringing an elevated homocysteine down to optimal levels, there are other interim interventions that can reduce its negative effects. Read on for more info.
Homocysteine in clinical practice
Homocysteine is one of the most prominent laboratory biomarkers used to assess methylation status. Although we never rely on just one indicator alone, this is one that we routinely assess in our patients presenting with a myriad of different symptoms and conditions.
We like to see homocysteine within a range of 4-7 nmol/mL. Both too little and too much can be problematic. In this article, we’re looking at one of the ways we address too much homocysteine, but you can read Dr. Fitzgerald’s thoughts on too little homocysteine here if you are interested.
Damage inflicted by too much homocysteine
Homocysteine is associated with cellular injury, specifically to the endothelial cells that line our blood vessels. For those familiar with the biology, homocysteine appears to exert stress on a cellular component called the endoplasmic reticulum, which creates reactive oxygen species and INFLAMMATION. We know that chronic inflammation can act both locally and on other parts of the body to damage tissue and cause problems.
Homocysteine may also negatively affect another cellular component, the mitochondria. These are crucial energy-producing organelles, producing the ubiquitously-used energy ‘currency’ called ATP (adenosine tri-phosphate). Reduced energy output, as you can imagine, has huge knock-on effects on nearly every other cellular function.
Disruptions in the methylation cycle can also influence levels of homocysteine’s precursor, s-adenosyl homocysteine, which may have even more potent effects than homocysteine and is known to block appropriate DNA methylation, which is crucial for proper gene regulation.
Methylation support reduces homocysteine
A good strategy for methylation support is appropriate for reducing an elevated homocysteine.
This is where we like to take a comprehensive diet and lifestyle approach as outlined
in our eBook, rather just singular B vitamin supplementation.
But what to do while you’re waiting for homocysteine to come down?
In the interim, research shows that there are several natural compounds, familiar to all Functional Medicine practitioners, which can attenuate the damaging effects of homocysteine on cellular function and our patient’s symptoms. These include:
MTHFR
Methylenetetrahydrofolate reductase (MTHFR) is an enzyme that converts 5,10-methylenetetrahydrofolate to 5,methyltetrahydrofolate, which is the active form of folate. Mutations in this gene cause the accumulation of homocysteine and a lack of available folate for cellular functions. Both of these factors have been linked to oxidative stress, vascular disease (including cardiovascular), neural tube defects, neurological disorders (including schizophrenia and bipolar disorder), cancer, preeclampsia, hypotonia, and seizures. Common mutations are rs1801133 (C677T), rs1801131 (A1298C), and rs2274976 (G1793A).
The C677T polymorphism is present in about 39% of caucasians as heterozygotes and 17% as homozygotes. Table 1 provides data on how much activity your MTHFR enzyme would possess with different combinations of the C677T and the A1298C. https://www.greatplainslaboratory.com/gpl-blog-source/2016/4/14/dna-methylation-pathway
The present review focuses on the B-vitamins, i.e. folate, vitamin B12, vitamin B6 and riboflavin, are involved in homocysteine metabolism. Homocysteine is a S-containing amino acid and its plasma concentrations can be raised by various constitutive, genetic and lifestyle factors, by inadequate nutrient status and as a result of systemic disease and various drugs. Hyperhomocysteinaemia is a modest independent predictor of CVD and stroke, however, causality and the precise pathophysiological mechanism(s) of homocysteine action remain unproven.
The predominant nutritional cause of raised plasma homocysteine in most healthy populations is folate insufficiency. Vitamin B12 and, to a lesser extent, vitamin B6 are also effective at lowering plasma homocysteine, especially after homocysteine lowering by folic acid in those individuals presenting raised plasma homocysteine.
However, riboflavin supplementation appears to be effective at lowering plasma homocysteine only in those individuals homozygous for the T allele of the C677T polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene. This gene codes for the MTHFR enzyme that produces methyltetrahydrofolate, which, in turn, is a substrate for the remethylation of homocysteine by the vitamin B12-dependent enzyme methionine synthase. Individuals with the MTHFR 677TT genotype are genetically predisposed to elevated plasma homocysteine, and in most populations have a markedly higher risk of CVD. https://www.ncbi.nlm.nih.gov/pubmed/15831132
But there is another dimension to the issue of depression. In the July, 2011 issue of Prevention Magazine (link is external), author Ginny Graves says that depression serves a purpose in our lives. Graves writes, ” ‘Depression may be nature‘s way of telling you to stop and focus on what’s troubling you, so you can move past it and get on with your life,’ says Paul Andrews, PhD, an evolutionary biologist at Virginia Commonwealth University.
He, along with colleague J. Anderson Thomson, MD, a staff psychiatrist at the Student Health Services and Institute of Law and Psychiatry at the University of Virginia, have become controversial proponents of an idea that actually dates back to Aristotle, that depression may lead to better mental health.”
These authors suggest that depression forces us to go inwards and ruminate on something that is problematic or troubling. In some cases, internally mulling over a painful experience can gradually lead to healing – what psychoanalysts often classify as “healthy mourning.” In some cases, however, just what we are mourning is not so clear, and we someone else to help us sort it out. Sometimes we also need the presence of another person to make it safe enough to mourn.
Key Topics covered during this presentation:
• Learn about methylation and methylation potential
• Discover how methylation potential is correlated with neurotransmitter balance
• Learn the significance of the methionine and homocysteine ratio
• See how the MTHFR gene affects homocysteine balance
• Understand patient methylation with the MethylDetox Profile https://cellsciencesystems.com/education/webinars/understanding-methylation-gene-regulation-and-the-methyldetox-profile/
Understanding Methylation, Gene Regulation and the MethylDetox …
