Japan’s life expectancy is 85 and that of the Philippines is 65.
Air pollution, lack of social and health services , lack of parks, libraries and activities to promote well being, congestion in the city, lack of garbage and sanitation in some areas, over population, lack of spaces to plant, lack of government support for farmers, lack of family planning, lack of health education and many more.
Every child born by a mother is minus 5 years from her life. A mother of 12 works as a housemaid, washing clothes till dawn. A father could not find a job. More children are born because of lack of access to family planning, condoms. In the USA , there is Planned parenthood where you can get free condoms.
What do you think are the factors that contributed to low life expectancy in the Philippines?
Is it the consumption of pork?
Is is second hand smoking?
Is it that the price of chicken is cheaper than the price of fish?
AD is a neurodegenerative disease of complex etiology (29, 30). The formation of neurofibrillary tangles (NFT), neuropil threads, and senile plaques have been implicated in the onset and development of the disease, but the relative causal weight of these and other factors in sporadic AD continues to be debated (30, 31). Although initiation and progression of AD may thus be multifactorial, it has been noted that incidence and regional distribution of NFT are most closely associated with the clinical manifestations of the disease (32, 33). NFT formation is the result of the accumulation of altered components of the neuronal cytoskeleton (34), and it has been suggested that “clogging” of neuronal processes and disruption of long-distance transport may underlie at least some of the cytopathological changes that characterize the disease (19).
We suggest that such cellular changes on one hand and deregulated expression and transport of dendritic RNAs on the other may be causally interrelated in AD. It has recently been speculated that non-protein-coding RNAs may be involved in AD (35), and we now show that expression of dendritic BC200 RNA, which is a translational repressor (3, 5), is differentially regulated in normal aging and in AD. In normal aging, BC200 levels in the neocortex decrease substantially after age 50. Because BC RNAs are prominently located throughout dendrites and at synapses (1, 2, 8), the substantial decline of BC levels may reflect the progressive atrophy of synaptodendritic structures that has previously been observed in normal aging (23, 36–39).
In AD, synapse loss and dendritic regression are substantial (40), but these degenerative changes are accompanied by significant dendritic sprouting and remodeling, often in the same neuron (30, 41, 42). Such reactive developments may be of a compensatory nature, directed at maintaining connectivity and plasticity. In one possible scenario, we therefore suggest that the substantially higher BC200 levels in AD, as compared with those in normal aging, may represent a molecular compensatory effort. If BC200 RNA is needed at the synapse for local translational control, its loss from synaptodendritic domains as the result of dendritic regression and clogging in AD may trigger compensatory mechanisms that result in the increased production of the RNA.
Increased synthesis of key synaptodendritic components may be an appropriate response in situations in which cargoes are not effectively delivered to postsynaptic sites. It may, at least initially or partially, be successful in overcoming moderate dendritic clogging that is caused by altered cytoskeletal components. Over time, however, such response may prove inadequate if further accumulation of cytoskeletal debris creates “roadblocks” that RNAs with dendritic destinations are no longer able to traverse. At this point, relative BC200 levels would begin to decrease in dendrites but increase in somata. In such cases, efforts to compensate would have failed because even increased production could no longer ensure that the RNA reaches its dendritic target sites. Transport deficits have previously been implicated in the progression of AD (18–20), and impaired microtubule-dependent transport, coupled with beginning axonal and dendritic blockage, may be an early event in AD that could eventually result in the local generation of amyloid-β peptides and thus in amyloid deposition (17).
Alternative scenarios are possible or even likely. Instead of, or in addition to, being reactive–compensatory to cytoskeletal degeneration, imbalances in the somatodendritic distribution of BC200 RNA could be causative because they may lead to aberrant local translational control. BC200 RNA contains a kink turn motif of the KT-58 subtype that has been implicated in dendritic transport of BC RNAs (9, 43). Because only slight perturbations of the kink turn motif architecture are sufficient to disrupt targeting (9), it is conceivable that single-nucleotide mutations in this region may prevent delivery of the RNA along the dendritic extent. Consequences would be twofold: compensatory elevation of BC200 transcription in an attempt to overcome dendritic delivery block and poor translational control in synaptodendritic domains. Consistent with this model, altered relative BC200 levels become manifest at a very early time point in the course of AD, possibly before clinical signs become detectable (44, 45).
A gradual worsening of somatodendritic BC200 imbalances may over time set off a self-reinforcing feed–forward cycle. Inadequate translational regulation in dendrites may lead to cytoskeletal overproduction and local dysfunction (16), which in turn would hinder the transport of mRNAs and protein synthetic machinery to postsynaptic target sites. In line with this concept, levels of somatodendritic RC3 mRNA have been shown to be significantly diminished in dendritic regions of AD brains (46). Having been disrupted in this manner, the system would find itself on a slow but accelerating course toward eventual catastrophe, manifesting as synaptic or plasticity failure (17, 30, 47–49). At the same time, increased perikaryal levels of BC200 RNA may inappropriately repress somatic protein synthesis and thus precipitate or exacerbate degenerative changes. We anticipate that future work, directed at the understanding of neuronal RNA transport and local translational control mechanisms, will be able to establish the respective contributions of the causative and reactive–compensatory scenarios.
The study samples come from the Adult Changes in Thought (ACT) study, a longitudinal research effort led by Eric B. Larson, M.D., M.P.H., and Paul K. Crane, M.D., M.P.H., of the Kaiser Permanente Washington Health Research Institute (KPWHRI) (formerly known as Group Health Research Institute) and the University of Washington School of Medicine to collect data on thousands of aging adults, including detailed information on their health histories and cognitive abilities.
“This collaboration with the Allen Institute for Brain Science has allowed us to gain insights never before possible into the relationships between neuropathology, gene expression, RNA quality, and clinical features tracked in the ACT study over more than 20 years,” says Larson, who has led the National Institute of Aging-supported study from its start in 1986 and is Vice President for Research and Health Care Innovation at Kaiser Permanente Washington.
During this generative sleep stage, the strengths of the feedforward synaptic … in the sense that only small changes are made during any one wake–sleep cycle. … sleep, the visual cortex is driven by brain-stem activity and the hippocampus …
This might be caused by the removal of tonic and phasic feed–forward … pool correlates with the duration of the oscillatory cycle, various brain rhythms can set …
So, to the degree that the hippocampal output during ripples originates in … in the prefrontal cortex and spreading through the whole neocortex and brain issue a … a feed forward manner favors the occurrence of another slow oscillation cycle …
J.A. Reggia, E. Ruppin, D.L. Glanzman – 1999 – Medical
… transmission in the piriform cortex, with a much weaker effect on feedforward … in the hippocampusgo much higher than ACh levels in neocortex (Marrosu et al., … rapid changes in modulatory dynamics within each cycle of the theta rhythm.
1): 1) feed–forward inhibition, in which excitatory inputs from extrinsic brain regions recruit local inhibitory … Feed–forward inhibition in neocortex and hippocampus …. This cycle then repeats to propagate seizure activity to the next microcircuit.
Ahn SM, Freeman WJ (1974) Steady-state and limit cycle activity of mass of … of functionally segregated circuits linking basal ganglia and cortex. … Alger BE, Nicoll RA (1982) Feed–forward dendritic inhibition in rat hippocampal pyramidal cells …
May 16, 2016 – The lateral entorhinal cortex (LEC) computes and transfers olfactory … Here we established LEC connectivity to upstream and downstream brain … RE+ neurons provide feedforwardprojections to the hippocampus while …… All animals were housed singly or in pairs and were kept on a 12 h light/dark cycle.
Christoph von der Malsburg, William A. Phillips, Wolf Singer – 2010 – Medical
From Neurons to Mind Christoph von der Malsburg, William A. Phillips, Wolf Singer … and Transfer at theHippocampus–Entorhinal– Neocortical Interface György Buzsáki … the multisynaptic feedforward loops of the entorhi- nal–hippocampal system, … In each oscillatory cycle, recruitment of principal neurons is temporally …
(A) Multiple loops of the hippocampal-entorhinal (EC) circuits. … computation in successive layers of the EC-hippocampus (mainly) feedforward loop. … the main direction of information flow, withneocortical– hippocampal transfer taking place … Neurons that discharge within the time period of the gamma cycle (10–30 msec) …
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Connie’s comments:
The plaque, clogging , RNA quality and rhythm of the brain circuits are affected by quality of life, whole foods, sleep, stress, and affected by toxins in our environment.
Knowing the effects of the clogging and plaques in our brain from stress, lack of sleep, toxins and inflammation that started in our intestines and environment (pollution, carbon monoxide poisoning, metal toxicities, others) can help us prevent Alzheimer’s. The cure is prevention 20 years before our brain can no longer clean up the plaques and clogs.
For quality supplementation to reset your gene expression to a younger you, visit:
Benzodiazepines Increase Mortality in Persons with Alzheimer’s Disease
Summary: Researchers report an elevated risk of death in Alzheimer’s patients who use benzodiazapines.
Source: University of Eastern Finland.
Benzodiazepine and related drug use is associated with a 40 per cent increase in mortality among persons with Alzheimer’s disease, according to a new study from the University of Eastern Finland. The findings were published in the International Journal of Geriatric Psychiatry.
The study found that the risk of death was increased right from the initiation of benzodiazepine and related drug use. The increased risk of death may result from the adverse events of these drugs, including fall-related injuries, such as hip fractures, as well as pneumonia and stroke.
The study was based on the register-based MEDALZ (Medication Use and Alzheimer’s Disease) cohort, which includes all persons diagnosed with Alzheimer’s disease in Finland during 2005-2011. Persons who had used benzodiazepines and related drugs previously were excluded from this study, and therefore, the study population consisted of 10,380 new users of these drugs. They were compared with 20,760 persons who did not use these drugs.
Although several treatment guidelines state that non-pharmacological options are the first-line treatment of anxiety, agitation and insomnia in persons with dementia, benzodiazepines and related drugs are frequently used in the treatment of these symptoms. If benzodiazepine and related drug use is necessary, these drugs are recommended for short-term use only. These new results encourage more consideration for benzodiazepine and related drug use in persons with dementia.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: Laura Saarelainen – University of Eastern Finland Publisher: Organized by NeuroscienceNews.com. Image Source: NeuroscienceNews.com image is credited to Singer et al., JNeurosci (2017). Original Research: Abstract for “Risk of death associated with new benzodiazepine use among persons with Alzheimer disease: A matched cohort study” by Laura Saarelainen, Anna-Maija Tolppanen, Marjaana Koponen, Antti Tanskanen, Jari Tiihonen, Sirpa Hartikainen, and Heidi Taipale in International Journal of Geriatric Psychiatry. Published online November 15 2017 doi:10.1002/gps.4821
Risk of death associated with new benzodiazepine use among persons with Alzheimer disease: A matched cohort study
Objective
To investigate the risk of death associated with new benzodiazepine and related drug (BZDR) use in a nationwide cohort of persons with Alzheimer disease (AD).
Methods
The register-based MEDALZ cohort, including all community-dwelling Finns diagnosed with AD during 2005 to 2011 (n = 70 718), was used. Clinically verified AD diagnoses were obtained from the Special Reimbursement Register. Drug use periods were modeled from BZDR purchases, derived from the Prescription Register. To study new users, persons who had any BZDR use during the year preceding the AD diagnosis were excluded.
For each person initiating BZDR use (n = 10 380), 2 nonusers (n = 20 760) were matched on age, gender, and time since AD diagnosis. The outcome was 180-day mortality, and BZDR use was compared with nonuse with Cox regression. Multivariable analyses were adjusted for Charlson comorbidity index, socioeconomic position, hip fractures, psychiatric disorders, substance abuse, stroke, and other psychotropic drug use.
Results
During the follow-up, 5 excess deaths per 100 person-years occurred during BZDR use in comparison to nonuse, and mortality rates were 13.4 (95% confidence interval [CI], 12.2-14.5) and 8.5 (95% CI, 7.9-9.1), respectively. Benzodiazepine and related drug use was associated with an increased risk of death (adjusted hazard ratio = 1.4 [95% CI, 1.2-1.6]), and the association was significant from the initiation of use. Benzodiazepine use was associated with an increased risk of death, whereas benzodiazepine-related drug use was not.
Conclusions
Benzodiazepine and related drug use was associated with an increased risk of death in persons with AD. Our results support treatment guidelines stating that nonpharmacological approaches should be the first-line option for symptomatic treatment of AD.
“Risk of death associated with new benzodiazepine use among persons with Alzheimer disease: A matched cohort study” by Laura Saarelainen, Anna-Maija Tolppanen, Marjaana Koponen, Antti Tanskanen, Jari Tiihonen, Sirpa Hartikainen, and Heidi Taipale in International Journal of Geriatric Psychiatry. Published online November 15 2017 doi:10.1002/gps.4821
Simple EKG Can Determine Whether Patient Has Depression or Bipolar Disorder
Summary: Heart rate variability can indicate whether a person has bipolar disorder or major depression, a new study reports.
Source: Loyola University Health System.
A groundbreaking Loyola Medicine study suggests that a simple 15-minute electrocardiogram could help a physician determine whether a patient has major depression or bipolar disorder.
Bipolar disorder often is misdiagnosed as major depression. But while the symptoms of the depressive phase of bipolar disorder are similar to that of major depression, the treatments are different and often challenging for the physician.
In bipolar disorder, formerly called manic depression, a patient swings between an emotional high (manic episode) and severe depression. Treatment for the depressed phase includes an antidepressant along with a safeguard such as a mood stabilizer or antipsychotic drug to prevent a switch to a manic episode. A physician who misdiagnoses bipolar disorder as major depression could inadvertently trigger a manic episode by prescribing an antidepressant without a safeguard mood stabilizing drug.
The study found that heart rate variability, as measured by an electrocardiogram, indicated whether subjects had major depression or bipolar disorder. (Heart rate variability is a variation in the time interval between heartbeats.) The study, by senior author Angelos Halaris, MD, PhD and colleagues, was published in the World Journal of Biological Psychiatry.
“Having a noninvasive, easy-to-use and affordable test to differentiate between major depression and bipolar disorder would be a major breakthrough in both psychiatric and primary care practices,” Dr. Halaris said. Dr. Halaris said further research is needed to confirm the study’s findings and determine their clinical significance.
Dr. Halaris is a professor in Loyola’s department of psychiatry and behavioral neurosciences and medical director of adult psychiatry.
Major depression is among the most common and severe health problems in the world. In the United States, at least 8 to 10 percent of the population suffers from major depression at any given time. While less common than major depression, bipolar disorder is a significant mental health problem, affecting an estimated 50 million people worldwide.
The Loyola study enrolled 64 adults with major depression and 37 adults with bipolar disorder. All subjects underwent electrocardiograms at the start of the study. Each participant rested comfortably on an exam table while a three-lead electrocardiogram was attached to the chest. After the patient rested for 15 minutes, the electrocardiographic data were collected for 15 minutes.
Using a special software package, researchers converted the electrocardiographic data into the components of heart rate variability. These data were further corrected with specialized software programs developed by study co-author Stephen W. Porges, PhD, of Indiana University’s Kinsey Institute.
In measuring heart rate variability, researchers computed what is known to cardiologists as respiratory sinus arrhythmia (RSA). At the baseline (beginning of the study), the subjects with major depression had significantly higher RSA than those with bipolar disorder.
In a secondary finding, researchers found that patients with bipolar disorder had higher blood levels of inflammation biomarkers than patients with major depression. Inflammation occurs when the immune system revs up in response to a stressful condition such as bipolar disorder.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
The study is titled “Low cardiac vagal tone index by heart rate variability differentiates bipolar from major depression.” In addition to Drs. Halaris and Porges, other co-authors are Brandon Hage, MD, a graduate of Loyola University Chicago Stritch School of Medicine now at the University of Pittsburgh (first author); Stritch student Briana Britton; Loyola psychiatric resident David Daniels, MD; and Keri Heilman, PhD of the University of North Carolina.
Source: Jim Ritter – Loyola University Health System Publisher: Organized by NeuroscienceNews.com. Image Source: NeuroscienceNews.com image is in the public domain. Original Research:Abstract for “Distinguishing bipolar II depression from unipolar major depressive disorder: Differences in heart rate variability” by Hsin-An Chang Department of Psychiatry, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Chuan-Chia Chang, Terry B. J. Kuo & San-Yuan Huang in World Journal of Biological Psychiatry. Published online November 14 2017 doi:10.3109/15622975.2015.1017606
Distinguishing bipolar II depression from unipolar major depressive disorder: Differences in heart rate variability
Objectives. Bipolar II (BPII) depression is commonly misdiagnosed as unipolar depression (UD); however, an objective and reliable tool to differentiate between these disorders is lacking. Whether cardiac autonomic function can be used as a biomarker to distinguish BPII from UD is unknown.
Methods. We recruited 116 and 591 physically healthy patients with BPII depression and UD, respectively, and 421 healthy volunteers aged 20–65 years. Interviewer and self-reported measures of depression/anxiety severity were obtained. Cardiac autonomic function was evaluated by heart rate variability (HRV) and frequency-domain indices of HRV.
Results. Patients with BPII depression exhibited significantly lower mean R–R intervals, variance (total HRV), low frequency (LF)-HRV, and high frequency (HF)-HRV but higher LF/HF ratio compared to those with UD. The significant differences remained after adjusting for age. Compared to the controls, the patients with BPII depression showed cardiac sympathetic excitation with reciprocal vagal impairment, whereas the UD patients showed only vagal impairment. Depression severity independently contributed to decreased HRV and vagal tone in both the patients with BPII depression and UD, but increased sympathetic tone only in those with BPII depression.
Conclusions. HRV may aid in the differential diagnosis of BPII depression and UD as an adjunct to diagnostic interviews.
“Distinguishing bipolar II depression from unipolar major depressive disorder: Differences in heart rate variability” by Hsin-An Chang Department of Psychiatry, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Chuan-Chia Chang, Terry B. J. Kuo & San-Yuan Huang in World Journal of Biological Psychiatry. Published online November 14 2017 doi:10.3109/15622975.2015.1017606
I am a retired Certified Ophthalmic Medical Technologist, so let me begin by giving you my “professional” opinion. Floaters were a common complaint I heard about, and this is what I used to tell patients. Some of it is actually good advice!
The eye has two compartments filled with different gel-like substances. At the front of the eye is aqueous, but the bulk of the eye is filled with vitreous, which is water and collagen, and it can break down as we age. When it breaks down it forms little bubbles and those bubbles cast a shadow on the retina, generating the appearance of dark spots floating around in the visual field. These spots are harmless and may fade, but will likely remain visible for the rest of your life. People tend to get used to them and they become less annoying. If it becomes so severe that it impairs the vision, there is a surgical technique to suck the vitreous out and replace it, but it is quite risky and expensive.
Floaters can be a very serious warning sign of a potentially blinding condition. If your floaters seem to form a web or a curtain, or if they are accompanied by flashes of light you need to get to an ophthalmologist IMMEDIATELY. The vitreous is adhered to the retina, and when the vitreous degrades it can pull the retina off. If you catch it early, the retina can be “tacked” back on with a laser quickly and almost painlessly. If it goes on too long, the retina requires major surgery and if it goes too far you loose the vision in that eye. There is no saving it once the retina peels off your macula (the central “sweet spot” of vision is processed there). If there is any pain, you ought to be checked out by a doctor. Floaters should never be painful.
Officially, and essentially, floaters themselves are harmless and there is no treatment, so get used to them. This is what I learned, and repeated many times. Then one day I got floaters and suddenly the advice I had given for decades was not adequate. I did go see an ophthalmologist. The risk of blindness is serious and I was not playing around. His assistant was a former co-worker who dutifully gave me the same advice I had been giving when I was a “professional” in the field. I was told my vitreous had not detached, but it probably would within the month based on my symptoms. Vitreous detachment is not as serious as retinal detachment, but can lead to a retinal detachment.
I am not a doctor, but I am more than willing to play one on myself, and so I applied my general knowledge of alternative healing to the problem. I figured I had two problems that needed to be addressed: 1) inadequate blood supply to my eye, and 2) collagen breakdown.
Improving the blood supply to my eye was a goal based on the simple premise that when there is decreased health in the tissues, it will boil down to the cells not getting enough oxygen. I went with citrus bioflavanoids, a supplement well known to strengthen blood vessels. To help build up collagen, I began taking glucosamine and chondroitan. Within 2 weeks, I cancelled my follow up appointment, the floaters had dissolved.
If you do not have access to these supplements, try a diet rich in the same nutrients. The white part of orange peels is an excellent source of bioflavanoids. But there are tastier sources like red bell peppers, garlic, and strawberries. Glucosamine and chondroitan are a bit trickier to get large doses of in your diet. I would make a good bone sauce, and a nice jambalaya where you eat the seafood – shells and all, and eat lots of them both.
Tips: Drink fresh juice of carrots, orange, pineapple and add turmeric powder. Deep breathing IN thru noise and out thru mouth. Sleep early and adequately. Detox parasites and fungus in the body. Get Vitamin D from the sun. Strengthen collagen and blood vessels with ginger, soft boiled eggs and Vitamin C. And more. Email motherhealth@gmail.com
Garlic is anti-bad-stuff. Viruses, fungi, bacteria, parasites, cancer, and vampires all hate garlic. It’s an absolutely amazing herb and the best in the business at killing bad stuff. It even chelates heavy metals (removes them from the body). Garlic is also a very powerful deterrent for blood sucking parasites like mosquitoes, ticks, and fleas.
Black Walnut-Nuts & Hull
The nuts and green hulls of black walnut (Juglans nigra) are loved by herbalists for their ability to cleanse the blood and the intestines. Black walnut hull is used to cure fungal infections. The juice from the green hulls are used to kill parasites. Only green hulls should be used.
Wormwood
Wormwood (Artemisia absinthium) is a perennial herb with tiny yellow-green flowers. Leaves and flowers are used to treat stomach problems and wormwood is a powerful remedy for intestinal worms. Wormwood should be avoided by women who or nursing. Wormwood has strong antimicrobial properties and is used for other infections as well.
Cloves
Clove essential oil is used to dissolve eggs found in the intestines that have been left behind by worms. It’s believed to be the only herb that actually does destroy almost all parasite eggs. When used in conjunction with black walnut and wormwood, the trio break the parasite’s life-cycles. Clove is also antibacterial, antiviral, and antifungal. Clove oil has powerful broad-spectrum antimicrobial properties.
Thyme
Thyme is one of the best herbs for stimulating the thymus, a major gland of the immune system. Thyme helps stimulate the body’s natural defenses and works very well with echinacea to boost the ability of our immune system. Oil of thyme can eliminate growth of many parasites, and it kills them in the intestinal tract.
Oil of Oregano
Oil of oregano is infused with extremely high levels of free-radical-crushing antioxidants, and it is antiparasitic, antiviral, antibacterial, and antifungal. It is a powerful, indiscriminate killer that can reset the microbial environment in the intestines. Many studies show the effectiveness of oil of oregano with everything from parasitical infections to cancer.
Chinese Goldthread
Goldthread (Coptis chinensis) has been used in traditional Chinese medicine for centuries to treat all types of infections, including bacterial, parasitic, yeast, and protozoan. It contains a substance called berberine, which is responsible for the broad-spectrum antimicrobial properties.
Diatomaceous Earth
Food grade diatomaceous earth absorbs methyl mercury, E. coli, endotoxins, viruses, organophosphate pesticide residues, and drug residues. Its positive effects include killing intestinal parasites, balancing the intestinal flora, killing viruses, and absorbing toxins. It’s great for intestinal cleanses. The only side effect known is its ability to irritate the lungs if inhaled; it is a very fine powder.
Cramp Bark Tea
Cramp bark is an herb often taken in tea form that can treat female problems like irritability and cramps associated with the menstrual cycle. The herb is hailed as a stomach cramp remedy in Russia, and helps to flush parasites from the body’s intestinal system. In addition to killing parasites, cramp bark can lower blood pressure and treat colds and coughing. Some cramp bark teas also include pumpkin seed extract, another anti-parasite herbal supplement that stunts the growth of intestinal worms. According to the University of Maryland, eating pumpkin seeds is an effective way to get rid of parasites.
Peppermint Tea
Peppermint tea is effective in treating intestinal parasites, and is also an herbal remedy for cramps and bloating. Peppermint also aids the salivary glands during the digestion process, and helps to relieve individuals suffering from bowel ailments. While peppermint has powerful antibacterial properties and can rid the body of parasites and other toxins, it’s best to consult a physician before drinking the herb tea on a regular basis, as taking conventional antifungal medications along with peppermint could cause toxic effects that intensify sickness.
Fennel Seed Tea
Fennel is a perennial herb ground into a tea; it is rich in potassium, zinc and vitamin C. Fennel tea can kill worms in the intestines and is also a natural treatment for diarrhea. According to The Brightest Hub website, fennel tea can also rid the body of infections like conjunctivitis, or pink eye. The tea will also act as a diuretic and flush excess liquid from the body, which includes toxins like parasites or worms. Fennel tea is an appetite suppressant, so some individuals use fennel along with other herbs or supplements for weight loss.
Hyssop Tea
Hyssop contains a hormone that makes the body more resistant to disease and can stop parasites from doing further damage in the body. The evergreen herb can be ground into a tea and is even mentioned several times in the Bible for its cleansing and purging properties. The tea has a minty flavor, and, aside from eliminating parasitic worms from the stomach, is an herbal remedy for fever blisters and bronchitis. Hyssop also helps to relieve anxiety and calm the nerves, and rids the body of phlegm and harmful fluids.
by Claire Cox
I am a retired Certified Ophthalmic Medical Technologist, so let me begin by giving you my “professional” opinion. Floaters were a common complaint I heard about, and this is what I used to tell patients. Some of it is actually good advice!
