Cancer

Cancer

Gut Bacteria (Pranic Footprint-प्राणमय कोष) controls speed of tumor growth

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I have shared it many times that the ultimate way of cancer prevention is to restore Prana in body. It is lack of prana/blockage of Nadi, that causes cancer.

Gut Bacteria, like any other body organ, is manifestation of Prana. And they being non-organ self of body, play critical role in well-being of body organs.

We can prevent cancer easily. Even cancer management is also less painful compare to modern chemo and radiation torture.

Three fundamental source of Prana for restoration

  1. Raw Prana from the Sun
  2. Churned Prana from Desi cow’s milk and ghee
  3. Food grown on the soil replenished by raw and churned prana (Sun light, cow dung, urine, milk, butter milk)

GUTBacteria


Research


Gut Bacteria Determine Speed of Tumor Growth in Pancreatic Cancer

https://nyulangone.org/press-releases/gut-bacteria-determine-speed-of-tumor-growth-in-pancreatic-cancer

The population of bacteria in the pancreas increases more than a thousand fold in patients with pancreatic cancer, and becomes dominated by species that prevent the immune system from attacking tumor cells.

These are the findings of a study conducted in mice and in patients with pancreatic ductal adenocarcinoma (PDA), a form of cancer that is usually fatal within two years. Led by researchers at NYU School of Medicine, Perlmutter Cancer Center, and NYU College of Dentistry, the study published online March 22 in Cancer Discovery, a journal of the American Association for Cancer Research (AACR).

Specifically, the study found that removing bacteria from the gut and pancreas by treating mice with antibiotics slowed cancer growth and reprogrammed immune cells to again “take notice” of cancer cells. Oral antibiotics also increased roughly threefold the efficacy of checkpoint inhibitors, a form of immunotherapy that had previously failed in pancreatic cancer clinical trials, to bring about a strong anti-tumor shift in immunity.

Experiments found that in patients with PDA, pathogenic gut bacteria migrate to the pancreas through the pancreatic duct, a tube that normally drains digestive juices from the pancreas into the intestines. Once in the pancreas, this abnormal bacterial mix (microbiome) gives off cellular components that shut down the immune system to promote cancer growth, say the authors.

Viral Infection : Sign of resilience, sign of life : Zika Virus kills Cancer cells

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Zika Cancer
I am not doctor but based on study and observation, I once told to my friends group that viral infections are indicators of healthy immune system. Don’t avoid them. Just take care of soothing and fast recovery.
 
Cancer is a stage indicating death. The last bastion for death to take over this body. Even dead-body flourishes like cancer after death. Difference between cancer and death is, presence of life/prana with body.
Old notes on : viral infections
———–
Research
———–

Zika virus kills brain cancer stem cells

Virus potentially could be used to treat deadly disease

While Zika virus causes devastating damage to the brains of developing fetuses, it one day may be an effective treatment for glioblastoma, a deadly form of brain cancer. New research from Washington University School of Medicine in St. Louis and the University of California San Diego School of Medicine shows that the virus kills brain cancer stem cells, the kind of cells most resistant to standard treatments.

The findings suggest that the lethal power of the virus – known for infecting and killing cells in the brains of fetuses, causing babies to be born with tiny, misshapen heads – could be directed at malignant cells in the brain. Doing so potentially could improve people’s chances against a brain cancer – glioblastoma – that is most often fatal within a year of diagnosis.

medicine.wustl.edu/news/zika-virus-kills-brain-cancer-stem-cells/

Onion and Cancer Prevention

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2765-onions

Some communities in India do not eat onion and garlic at all (For spiritual reasons and to avoid TAMAS nature and remain sattvik). Imagine what they miss.

As per research, onions work for preventing and curing cancer.

Have you ever seen farm labor or construction labor inflicted by cancer?

No. They have onion in diet and they do hard-work 🙂.

“As per Ayurveda, who does physical work has to eat onion. if our work profile does not allow us to do physical work then TAMAS will increase if eaten onion.” – Dhruv Dave

Modern science experiments don’t talk about conditions 🙂.

Summer is approaching. Eat onions. Since many of us do not do hard work, it is must for us to do exercise so that onion can work.

Only eating onions won’t work.


Research


Inhibitory effects of onion (Allium cepa L.) extract on proliferation of cancer cells and adipocytes via inhibiting fatty acid synthase.

Onion Kills 85% of Breast Cancer Cells in Vitro: An extract of onions was shown to kill up to 85% of aggressive, triple-negative breast cancer cells in vitro in this study. It also dramatically slowed the cancer cell’s growth by 84%, by shutting down their ability to manufacture fatty acids. But can onions reduce breast cancer risk in women? Yes, according to a study out of Italy where women consuming at least one serving of onions daily saw a 25% reduction in breast cancer risk (one serving = 3 ounces or 80 grams). That same dosage also reduced ovarian cancer risk by 73%. Why are onions so powerful? They contain thiosulfinates (sulfur-based compounds which potently inhibit cancer) and they are also a uniquely concentrated source of healthy 4-Oxo-flavonoids: only kale, black currants and the herb sage deliver as much per ounce! Onions may have further health benefits as well: they have lowered blood sugar in diabetic patients in one study, and in a recent clinical trial, overweight women eating 50-60 grams daily of raw red onion actually saw their cholesterol levels drop significantly. Onions are low in calories, are easy to include in a healthy diet in salads, soups, omelettes, sandwiches, even smoothies. Note: just as raw garlic is better than cooked for fighting cancer, raw onion is likely to offer the most benefit (both are allium vegetables).

https://www.ncbi.nlm.nih.gov/pubmed/23317220

Prolonged Work-Stress and Cancer

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Stress

Many friends ask me, why Indians used to live short life despite having rich Ayurvedic knowledge?

“Short life span was not pan-India observation. It was limited to British ruled area. And it is because Indians under British lived slave’s life. Slaves live under stress. Stress accelerates aging. Stress kills. Many remote villages unaffected by British rule, did have long life span as it is observed now”

👆 Work stress = Cancer or TB any chronic disease

Good Morning. Read it. Slow down. Our mindless race to achieve something (which many don’t realize) virtual (career, growth, money) beyond our capacity induces stress. This does not mean we don’t pursue our goals. It only mean, pursue without generating stress on body and mind. Stress , as I shared with friends often, is root cause of inflammation and inflammation a root cause of cancer. This research proves my hypothesis about stress.

Avoid work stress for your family sake


Research


http://www.inrs.ca/english/actualites/prolonged-exposure-work-related-stress-thought-be-related-certain-cancer

Prolonged exposure to work-related stress thought to be related to some cancers

For men, prolonged exposure to work-related stress has been linked to an increased likelihood of lung, colon, rectal, and stomach cancer and non-Hodgkin lymphoma. The findings are among the results obtained by researchers at INRS and Université de Montréal who conducted the first study to assess the link between cancer and work-related stress perceived by men throughout their working life. The research results were recently published in Preventive Medicine.
On average, the study participants had held four jobs, with some holding up to a dozen or more during their working lifetime. Significant links to five of the eleven cancers considered in the study were revealed. These links were observed in men who had been exposed to 15 to 30 years of work-related stress, and in some cases, more than 30 years. A link between work-related stress and cancer was not found in participants who had held stressful jobs for less than 15 years.
The most stressful jobs included firefighter, industrial engineer, aerospace engineer, mechanic foreman, and vehicle and railway-equipment repair worker. For the same individual, stress varied depending on the job held. Researchers were able to document changes in perceived work-related stress.
The study also shows that perceived stress is not limited to high work load and time constraints. Customer service, sales commissions, responsibilities, the participant’s anxious temperament, job insecurity, financial problems, challenging or dangerous work conditions, employee supervision, interpersonal conflict, and a difficult commute were all sources of stress listed by the participants.
“One of the biggest flaws in previous cancer studies is that none of them assessed work-related stress over a full working lifetime, making it impossible to determine how the duration of exposure to work-related stress affects cancer development. Our study shows the importance of measuring stress at different points in an individual’s working life,” explain the authors of the study.
The results obtained raise the question of whether chronic psychological stress should be viewed as a public health issue. But these results are as yet unsubstantiated because they are based on a summary assessment of work-related stress for a given job. There is now a need for epidemiological studies based on reliable stress measurements, repeated over time and that take all sources of stress into account.

Microbes and Cruciferous Vegetables : Cancer Cure

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It confirms once more that:

  1. the inflamed organs end into cancer
  2. Prana heals (Here, in form of microbes that releases chemical to stop the cancer proliferation signals

Cruciferos-Vegetable


Research


With these special bacteria, a broccoli a day can keep the cancer doctor away

Colorectal cancer is one of the most common cancers in the world, especially the developed world. Although the 5-year survival rates for earlier stages of this cancer are relatively good, at later stages survival goes down and the risk of cancer recurrence goes up considerably.

At the heart of this cancer-targeting system is an engineered form of E. coli Nissle, a harmless type of bacteria found in the gut. Using genetic techniques, the team engineered the bacteria into a probiotic that attached to the surface of colorectal cancer cells and secreted an enzyme to convert a substance found in cruciferous vegetables (like broccoli) into a potent anticancer agent. The idea was for the cancer cells in the vicinity to take up this anticancer agent and be killed. Normal cells cannot do this conversion, nor are they affected by the toxin, thus the system should be targeted only to colorectal cancer cells.

True enough, the mixture of engineered probiotics with a broccoli extract or water containing the dietary substance killed more than 95% of colorectal cancer cells in a dish. Moreover, the mixture had no effect on cells from other types of cancer such as breast and stomach cancer. Strikingly, the probiotics-veggie combination reduced tumour numbers by 75% in mice with colorectal cancer. Also, the tumours that were detected in these mice were 3 times smaller than those in control mice which were not fed with the mixture.

https://www.nature.com/articles/s41551-017-0181-y

Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4432495/

Significance: Sulforaphane, produced by the hydrolytic conversion of glucoraphanin after ingestion of cruciferous vegetables, particularly broccoli and broccoli sprouts, has been extensively studied due to its apparent health-promoting properties in disease and limited toxicity in normal tissue. Recent Studies: Recent identification of a sub-population of tumor cells with stem cell-like self-renewal capacity that may be responsible for relapse, metastasis, and resistance, as a potential target of the dietary compound, may be an important aspect of sulforaphane chemoprevention. Evidence also suggests that sulforaphane may target the epigenetic alterations observed in specific cancers, reversing aberrant changes in gene transcription through mechanisms of histone deacetylase inhibition, global demethylation, and microRNA modulation. Critical Issues: In this review, we discuss the biochemical and biological properties of sulforaphane with a particular emphasis on the anticancer properties of the dietary compound. Sulforaphane possesses the capacity to intervene in multistage carcinogenesis through the modulation and/or regulation of important cellular mechanisms. The inhibition of phase I enzymes that are responsible for the activation of pro-carcinogens, and the induction of phase II enzymes that are critical in mutagen elimination are well-characterized chemopreventive properties. Furthermore, sulforaphane mediates a number of anticancer pathways, including the activation of apoptosis, induction of cell cycle arrest, and inhibition of NFκB. Future Directions: Further characterization of the chemopreventive properties of sulforaphane and its capacity to be selectively toxic to malignant cells are warranted to potentially establish the clinical utility of the dietary compound as an anti-cancer compound alone, and in combination with clinically relevant therapeutic and management strategies. Antioxid. Redox Signal. 22, 1382–1424.

Fatty Acids Or Lipids, Estrogen and Cancer

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Highfat estrogen

Everyone knows that modern high-fat processed diet lead to obesity. Obesity is associated with several health issues, including cancer.

But since this fact is popular, even doctors, now prescribe low-fat diet. They force patients to get rid of even traditional fat-focused diet like Ghee.

At this juncture, it is important to know different dietary fat and their role in health and diseases.

Different Types of Dietary Fats

Fatty acids are long, straight-chain molecules categorized as:

  1. Saturated : Animal far
  2. Monosaturated
  3. Polyunsaturated

Difference between them is their chemistry. Since our focus is cancer, we will consider only those fat types which affects cancer etiology upto some extent (In reality, there is no single cause for cancer. There are always multiple factors working together, causing cancer).

Omega-6 fat, Estrogen and Cancer

In 1982, National research council, USA, identified fats (Omega-6 fatty acids) as the single dietary component most strongly related to cancer risk. This report was based on studies that suggested correlations between fats consumption and incidence of GI, Prostate and breast cancers.

But these reports did not provide specific detail. Later it was realized from more studies that intake of omega-6 fatty acids may promote cancer progression partly by increasing the production of availability of estrogen. [1][2][3][4][5][6]

Estrogen is a growth factor for a number of cancers, including breast cancer. High-fat diets and associated increase in fat tissuecan increase estrogen by number of ways:

  1. Fat tissue is a major source of estrogen production in postmenopausal women.
  2. Obesity and insulin resistance can decrease the levels of sex hormone binding globulin in men and women and increase cancer risk. Decreased binding protein means more biologically active estrogen.
  3. Obesity can alter estrogen metabolism in the liver
  4. High-fat diet may reduce the amount of estrogen excreted through the feces.

If you have not read old post, we have covered here (http://prachodayat.in/fast-food-estrogen-storm/), how fast-food diet leads to high serum estrogen level. And as per this post, it plays critical role in cancer progression.

Make your teen kids aware about this and help them love their life. Stop being suicidal. Stop fast food, processed food and high-fat diet full of Omega-6 fat.

Solution is to replace Omega-6 fat by Omega-3 fat. In Indian context, it is desi cow ghee.

 


References


[1] Dwyer JT. Dietary fat and breast cancer: Testing interventions to reduce risks. In Exercise, calories, fat and cancer. Jacobs MM, ed. New York: Plenum Press, 1992.

[2]

Possible Mechanisms through which Dietary Lipids, Calorie Restriction, and Exercise Modulate Breast Cancer

Though the exact cause of breast cancer still remains a mystery, years of investigations have suggested that several dietary and endocrine-related factors may induce and/or could modulate the growth of breast cancer. Epidemiologic and experimental evidence have indicated a close association between high-fat diets and increased incidence of breast cancer.1–3 Furthermore, several immunologic functions, including the levels of growth factors, cytokines, and sex steroid hormones, may be altered or regulated by dietary lipids.4,5 Excessive fat in the diet has been reported to enhance the growth of both spontaneously occurring and chemically induced colon and mammary tumors, as well as accelerated growth of transplantable carcinomas.6–8 Diets containing high levels of ω-6 fatty acids derived from vegetable fats appear to enhance tumorigenesis, while ω-3-containing lipids, either from vegetable or marine origin, or low levels of fat in the diet can diminish tumorigenesis. Recently, a number of mechanisms have been proposed to explain the modulation of mammary tumorigenesis in experimental animals by increasing the levels of dietary fats.9,10 Initiation and promotion have been linked to immune suppression,11 prostaglandin production,12,13 free radical formation,14 membrane fluidity changes,15 intracellular transport system modulation,16 increased caloric utilization,17 increased mammotrophic hormone secretion,18and cytokine changes.19,20 Over-expression of oncogenes and certain growth factors are other mechanisms that have been linked to dietary changes that may influence mammary tumori-genesis.

https://link.springer.com/chapter/10.1007%2F978-1-4684-7953-9_15

[3]

Meta-analysis: Dietary Fat Intake, Serum Estrogen Levels, and the Risk of Breast Cancer

Abstract

BACKGROUND: There is compelling evidence that estrogens influence breast cancer risk. Since the mid-1980s, dietary fat intervention studies have been conducted to investigate the effect of fat intake on endogenous estrogen levels. To further our understanding of the possible relationship between dietary fat and breast cancer, we conducted a meta-analysis of dietary fat intervention studies that investigated serum estradiol levels, and we reviewed the nature of the evidence provided by prospective analytic studies of fat consumption and breast cancer risk. METHODS: A computerized search of the English language literature on estrogen/estradiol and dietary fat intervention studies published from January 1966 through June 1998 was conducted using the MEDLINE® database. Pooled estimates were derived from the change in estradiol levels associated with fat reduction from 13 studies. Analyses were conducted separately for premenopausal and postmenopausal women and in both groups combined. RESULTS AND CONCLUSIONS: Statistically significant reductions in serum estradiol levels of − 7.4% (95% confidence interval [CI] = − 11.7% to −2.9%) among premenopausal women and − 23.0% (95% CI = −27.7% to −18.1%) among postmenopausal women were observed, with an overall −13.4% (95% CI = −16.6% to −10.1%) reduction observed. The greatest reductions occurred in two studies in which dietary fat was reduced to 10%-12% of calories compared with 18%-25% of calories in the other studies. A statistically significant reduction in estradiol levels of −6.6% (95% CI = −10.3% to −2.7%) remained after exclusion of these two studies. Review of prospective analytic epidemiologic studies that allowed for dietary measurement error suggests that the possibility that reducing fat consumption below 20% of calories will reduce breast cancer risk cannot be excluded. IMPLICATIONS: Dietary fat reduction can result in a lowering of serum estradiol levels and such dietary modification may still offer an approach to breast cancer prevention.

https://academic.oup.com/jnci/article/91/6/529/2549361

[4]

Western nutrition and the insulin resistance syndrome: a link to breast cancer.

https://www.ncbi.nlm.nih.gov/pubmed/10099938

[5] https://www.ncbi.nlm.nih.gov/pubmed/8391818

[6]

Sex hormone-binding globulin, its membrane receptor, and breast cancer: a new approach to the modulation of estradiol action in neoplastic cells.

The role of human Sex Hormone-Binding Globulin (SHBG), the plasma carrier of sex steroids, and its membrane receptor, SHBG-R, in estrogen-dependent breast cancer has been investigated in our laboratory in the past few years. SHBG-R is expressed in MCF-10 A cells (not neoplastic mammary cells), MCF-7 cells (breast cancer, ER positive) and in tissue samples from patients affected with ER positive breast cancer, but not in estrogen-insensitive MDA-MB 231 cells. The SHBG/SHBG-R interaction, followed by the binding of estradiol to the complex protein/receptor, causes a significant increase of the intracellular levels of cAMP, but does not modify the amount of estradiol entering MCF-7 cells. The estradiol-induced proliferation of MCF-7 cells is inhibited by SHBG, through SHBG-R, cAMP and PKA. Similarly, the proliferation rate of tissue samples positive for SHBG-R was significantly lower than the proliferation rate of negative samples. SHBG and SHBG-R could thus trigger a ‘biologic’ anti-estrogenic pathway. In order to get a more detailed knowledge of this system, we first examined the frequence of the reported mutated form of SHBG in 255 breast cancer patients. The mutated SHBG is characterized by a point mutation (Asp 327 –> Asn) causing an additional N-glycosylation site, which does not affect the binding of steroids to SHBG. The frequence of the mutation was significantly higher (24.5%) in estrogen-dependent breast cancers than in healthy control subjects (11.6%). This observation confirms the close relationship between SHBG and estrogen-dependent breast cancer and suggests that the mutation could modify SHBG activity at cell site. Lastly, the possibility of using SHBG to modulate the estradiol action in breast cancer was further studied by transfecting MCF-7 cells with an expression vector carrying the SHBG cDNA (study in collaboration with G.L. Hammond). Transfected cells are able to produce significant amount of SHBG in their medium, but their SHBG-R is reduced to undetectable levels. The SHBG produced by transfected MCF-7 cells is, however, able to inhibit estradiol-induced proliferation of MCF-7 cells expressing a functional receptor. Thus, the local production of SHBG obtained with transfection could be a useful tool to control cell growth in estrogen-dependent breast cancer.

https://www.ncbi.nlm.nih.gov/pubmed/10419027

Pill Now? Cancer Later

Pills

Don’t panic if you have taken in past. Avoid in future and take measures to reverse the effect in body by living stress-free life.

I have been vocal against idiotic Pill obsession. Mindless birth control pills in your young age will invite grave danger in menopausal age. Not only obesity but also diabetes, cancer and hormonal disorders.

It is grave mistake on govt side to promote contraceptives as birth control tools.

Not only females, newborns also suffer due to pills. Early in fetal life, nutrient deficiencies may result in severe impairments. For example, folate. Or as popularly known as : B Vitamin. Pill obsession will make your child devoid of folate in growth period as mother’s folate level reduces due to pill-intake.

Take care. Spread awareness. Save Nation.

ACCORDING TO A LOT OF DOCTORS:

Got acne? Take the pill.
Got PMS? Take the pill.
Got irregular cycles? Take the pill.
Don’t want to get pregnant? Take the pill.

All thanks parents’ pre-planning sexual indulgence and avoidance of progeny by modern pills. Folate is a vitamin that may become depleted with the use of birth control pills. Aside from the long list of potential side effects birth control pills can deplete important nutrients. These nutrients include: Vitamin B2, Vitamin B6, Vitamin B12, Folic Acid, Vitamin C, Magnesium and Zinc.

Once the pills become regular bedroom utility, body start denying absorption of nutrients. No matter how sophisticated supplements you take.

Such information is never passed-on to teens and young married couples. And so sex becomes pleasure machine for them. Instant, handy and under control. What a toxic delusion! 🙁🙁 And and top of that Idiot Chetan Bhagat tribe cry for porn freedom rights!! Ghor Kaliyug !! 🙁🙁

Spread the awareness. Save the future of Bharat.

More here : http://prachodayat.in/belong-pill-tribe/

 


Research


Contemporary Hormonal Contraception and the Risk of Breast Cancer

http://www.nejm.org/doi/full/10.1056/NEJMoa1700732

Background

Little is known about whether contemporary hormonal contraception is associated with an increased risk of breast cancer.

Methods

We assessed associations between the use of hormonal contraception and the risk of invasive breast cancer in a nationwide prospective cohort study involving all women in Denmark between 15 and 49 years of age who had not had cancer or venous thromboembolism and who had not received treatment for infertility. Nationwide registries provided individually updated information about the use of hormonal contraception, breast-cancer diagnoses, and potential confounders.

Results

Among 1.8 million women who were followed on average for 10.9 years (a total of 19.6 million person-years), 11,517 cases of breast cancer occurred. As compared with women who had never used hormonal contraception, the relative risk of breast cancer among all current and recent users of hormonal contraception was 1.20 (95% confidence interval [CI], 1.14 to 1.26). This risk increased from 1.09 (95% CI, 0.96 to 1.23) with less than 1 year of use to 1.38 (95% CI, 1.26 to 1.51) with more than 10 years of use (P=0.002). After discontinuation of hormonal contraception, the risk of breast cancer was still higher among the women who had used hormonal contraceptives for 5 years or more than among women who had not used hormonal contraceptives. Risk estimates associated with current or recent use of various oral combination (estrogen–progestin) contraceptives varied between 1.0 and 1.6. Women who currently or recently used the progestin-only intrauterine system also had a higher risk of breast cancer than women who had never used hormonal contraceptives (relative risk, 1.21; 95% CI, 1.11 to 1.33). The overall absolute increase in breast cancers diagnosed among current and recent users of any hormonal contraceptive was 13 (95% CI, 10 to 16) per 100,000 person-years, or approximately 1 extra breast cancer for every 7690 women using hormonal contraception for 1 year.

Conclusions

The risk of breast cancer was higher among women who currently or recently used contemporary hormonal contraceptives than among women who had never used hormonal contraceptives, and this risk increased with longer durations of use; however, absolute increases in risk were small. (Funded by the Novo Nordisk Foundation.)

For 50 years, Sugar Industry cartel hid the link between Processed Sugar and Cancer

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Sugar Cancer

When a like-minded friend shared below comment with me, I started thinking about the correlation.

 “It looks like Sugar is doing all the Vata Disorder even in remote areas like hilly states of Uttarakhand and Himachal.

Thyroid disorders, blood pressure, heart attack, diabtes in remote areas is unjustifiable. 
Sugar is taking a great toll”

I think my friend is right. If you observe last 20-25 years, due to easy road transport technology and electricity everywhere, modern utensils and processed food has reached even remote area. They did play critical role in bringing life-style disorders to the remote hill area.

Tips from personal experience, learning and observations:

  1. Avoid processed polished sugar in regular diet
  2. Best if you can stop having it
  3. Replace sugar by jaggery prepared without chemicals
  4. Unprocessed Sugar – once in a while

Here are  research paper showing how sugar industry never allowed to publish health impact reserch.


Sugar industry sponsorship of germ-free rodent studies linking sucrose to hyperlipidemia and cancer: An historical analysis of internal documents

https://doi.org/10.1371/journal.pbio.2003460


In 1965, the Sugar Research Foundation (SRF) secretly funded a review in the New England Journal of Medicine that discounted evidence linking sucrose consumption to blood lipid levels and hence coronary heart disease (CHD). SRF subsequently funded animal research to evaluate sucrose’s CHD risks. The objective of this study was to examine the planning, funding, and internal evaluation of an SRF-funded research project titled “Project 259: Dietary Carbohydrate and Blood Lipids in Germ-Free Rats,” led by Dr. W.F.R. Pover at the University of Birmingham, Birmingham, United Kingdom, between 1967 and 1971. A narrative case study method was used to assess SRF Project 259 from 1967 to 1971 based on sugar industry internal documents. Project 259 found a statistically significant decrease in serum triglycerides in germ-free rats fed a high sugar diet compared to conventional rats fed a basic PRM diet (a pelleted diet containing cereal meals, soybean meals, whitefish meal, and dried yeast, fortified with a balanced vitamin supplement and trace element mixture). The results suggested to SRF that gut microbiota have a causal role in carbohydrate-induced hypertriglyceridemia. A study comparing conventional rats fed a high-sugar diet to those fed a high-starch diet suggested that sucrose consumption might be associated with elevated levels of beta-glucuronidase, an enzyme previously associated with bladder cancer in humans. SRF terminated Project 259 without publishing the results. The sugar industry did not disclose evidence of harm from animal studies that would have (1) strengthened the case that the CHD risk of sucrose is greater than starch and (2) caused sucrose to be scrutinized as a potential carcinogen. The influence of the gut microbiota in the differential effects of sucrose and starch on blood lipids, as well as the influence of carbohydrate quality on beta-glucuronidase and cancer activity, deserve further scrutiny.


Supporting research material


Scientists’ Study Sweetens Connection Between Cancer, Sugar

http://www.utdallas.edu/news/2017/5/30-32567_Scientists-Study-Sweetens-Connection-Between-Cance_story-wide.html?WT.mc_id=NewsHomePageCenterColumn

Excessive sugar consumption is not only a problem that can lead to complications like diabetes, but also, based on our studies and others, the evidence is mounting that some cancers are also highly dependent on sugar.

Dr. Jung-whan “Jay” Kim,
assistant professor
of biological sciences

 

“As a culture, we are very addicted to sugar,” Kim said. “Excessive sugar consumption is not only a problem that can lead to complications like diabetes, but also, based on our studies and others, the evidence is mounting that some cancers are also highly dependent on sugar. We’d like to know from a scientific standpoint whether we might be able to affect cancer progression with dietary changes.”

The research was supported by the National Institutes of Health, the American Lung Association, the Japan Agency for Medical Research and Development, the Takeda Science Foundation, the Welch Foundation and the Cancer Prevention and Research Institute of Texas.

The research team, which included a Dallas high school student who interned in Kim’s lab, first tapped into a large government database called The Cancer Genome Atlas, which maps information about 33 types of cancer gathered from more than 11,000 patients.

Based on that data, they found that a protein responsible for transporting glucose — a kind of sugar — into cells was present in significantly higher levels in lung SqCC than in lung ADC. The protein, called glucose transporter 1, or GLUT1, takes up glucose into cells, where the sugar provides a fundamental energy source and fuels cell metabolism. GLUT1 is also necessary for normal cell functions, such as building cell membranes.

“Prior to this study, it was thought that the metabolic signatures of these two types of lung cancers would be similar, but we realized that they are very different,” Kim said. “These findings lend credence to the idea that cancer is not just one disease, but many diseases that have very different characteristics.”

With elevated GLUT1 implicated in SqCC’s appetite for sugar, the researchers looked for additional evidence by examining human lung tissue and isolated lung cancer cells, as well as animal models of the disease.

 

Sugar in Western diets increases risk for breast cancer tumors and metastasis

https://www.mdanderson.org/newsroom/2015/12/sugar-in-western-diets.html

“We found that sucrose intake in mice comparable to levels of Western diets led to increased tumor growth and metastasis, when compared to a non-sugar starch diet,” said Peiying Yang, Ph.D., assistant professor of Palliative, Rehabilitation, and Integrative Medicine. “This was due, in part, to increased expression of 12-LOX and a related fatty acid called 12-HETE.”

Previous epidemiological studies have shown that dietary sugar intake has an impact on breast cancer development, with inflammation thought to play a role.

“The current study investigated the impact of dietary sugar on mammary gland tumor development in multiple mouse models, along with mechanisms that may be involved,” said co-author Lorenzo Cohen, Ph.D., professor of Palliative, Rehabilitation, and Integrative Medicine. “We determined that it was specifically fructose, in table sugar and high-fructose corn syrup, ubiquitous within our food system, which was responsible for facilitating lung metastasis and 12-HETE production in breast tumors.”

Cohen added that the data suggested that dietary sugar induces 12-LOX signaling to increase risks for breast cancer development and metastasis.

Identifying risk factors for breast cancer is a public health priority, say the authors.  The researchers state that moderate sugar consumption is critical, given that the per capita consumption of sugar in the U.S. has surged to over 100 lbs. per year and an increase in consumption of sugar-sweetened beverages has been identified as a significant contributor to an epidemic of obesity, heart disease and cancer worldwide.

Cancer and Death : Two Biological events

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Would you call ‘Death’ as disease? No, right? Death is not a disease. It is biological event. Similarly, cancer is also a biological event. Sometimes, it surfaces on life early. Most of the times, it does in last stage of life. Game of circadian clocks. Time driven events.

diagram-showing-how-cancer-cells-keep-on-reproducing-to-form-a-tumour_0

Cancer is a property of each cell. It is the faulty clock that leads to cell into Cancer pathway than Cell Death pathway.

We all take birth with a probability of normal cells turned cancer cells.

Once you die, the cells in your body think that you are an embryo….so all the genes which remain up in embryo (and that never again become active in your life time after birth) become active again.

Body cells also think that there is something wrong, that’s why there is no signal of cell proliferation, development etc. So, the cells start expressing the genes that are generally overexpressed during cancer. I.e. signal is given to cell to proliferate (multiply).

People who get organ donation from dead body are more prone to cancers. This is explanation!!
Or in other words, Cancer is a sign of early death or rapid aging.

 


Research


http://www.scripps.edu/news/press/2016/20161116lamia.html

TSRI Researchers Show How Circadian ‘Clock’ May Influence Cancer Pathway

A new study led by scientists at The Scripps Research Institute (TSRI) describes an unexpected role for proteins involved with our daily “circadian” clocks in influencing cancer growth.

The research, published recently in the journal Molecular Cell, suggests that disruptions in circadian rhythms might leave levels of an important cancer-linked protein, called cMYC, unchecked.

“This appears to have big implications for the connection between circadian rhythms and cancer,” said TSRI biologist Katja Lamia, senior author of the study.

There is growing evidence that shift work and frequent jet lag can raise a person’s risk of cancer, suggesting a link between daily rhythms and cell growth. “We know this connection exists, but we haven’t known why,” said Lamia.

The researchers focused on proteins called cryptochromes, which evolved from bacterial proteins that sense light and repair DNA damage caused by sunlight. In humans, these proteins, called CRY1 and CRY2, regulate our circadian clocks, which influence what times of day we become tired, hungry and much more.

Using cells from mouse models, the researchers demonstrated that deleting the gene that expresses CRY2 reduced the cells’ ability to degrade a protein called cMYC. Without CRY2 keeping cMYC at normal levels, the researchers saw increased cell proliferation—similar to the abnormal growth seen in cancers.

Further studies of protein structures suggested that CRY2 is a key player in a process to “mark” cMYC for degradation. The researchers said it is significant that this process occurs after gene transcription—once the proteins are already produced—rather than during transcription, as in many other cryptochrome functions.

“This is a function of a circadian protein that has never been seen before,” said TSRI Research Associate Anne-Laure Huber, who served as first author of the study.

The researchers say more studies are needed to confirm this connection between circadian clocks and cancer in human tissues.

In addition to Lamia and Huber, authors of the study, “CRY2 and FBXL3 Cooperatively Degrade c-MYC,” were Stephanie J. Papp, Alanna B. Chan, Sabine D. Jordan, Anna Kriebs and Madelena Nguyen of TSRI; Emma Henriksson of TSRI and Lund University; Martina Wallace and Christian M. Metallo of the University of California, San Diego; and Zhizhong Li of the Genomics Institute of the Novartis Research Foundation and Novartis Institutes for Biomedical Research.

This study was supported by the National Institutes of Health (grants DK090188, DK097164, CA188652 and NIGMS P41-GM103311), the Searle Scholars Program through the Kinship Foundation, the Sidney Kimmel Foundation, the Lung Cancer Research Foundation, the Swedish Research Council, the Deutsche Forschungsgemeinschaft and the American Heart Association (grant 15POST22510020).

 

 

Ginger :10000 times more effective than Chemotherapy

1

Ginger Cancer

What is cancer cell?

Some dirty cell of your body? No. This body is wonderful gift. Nature does not act dirty. You and me do. Cancer cell is ordinary cell with cancerous tendency. Such tendency is expected due to cellular level stress. This stress is due to mental stress, physical stress (Food, water, air pollution) and environmental stress. Prolonged stress.

No cell loves to act cancerously. If you help them reduce local and global stress, they prefer to live happy life for you.

Cancer stem cells is a step before Cancer Cells. Cancer stem cells (CSCs) pose a serious obstacle to cancer therapy as they can be responsible for poor prognosis and tumour relapse.

It is shown by this research paper that Ginger compounds act against CSCs and inhibits them.

So is this the solution? No! Why should we even invite cancer? Prevention is always better than cure. Having ginger in diet can help but more than that stress-free life is more important! The root of all sicknesses start with weak mind!

Beware! Ginger and Turmeric are found 10000 times more effective than Chemotherapy. Now, we will have flood industrial farming of ginger and turmeric. That will follow genetically modified Ginger and Turmeric. That is how species are destroyed by Idiot science.


Research


6-Shogaol Inhibits Breast Cancer Cells and Stem Cell-Like Spheroids by Modulation of Notch Signaling Pathway and Induction of Autophagic Cell Death

http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0137614

Abstract

Cancer stem cells (CSCs) pose a serious obstacle to cancer therapy as they can be responsible for poor prognosis and tumour relapse. In this study, we have investigated inhibitory activity of the ginger-derived compound 6-shogaol against breast cancer cells both in monolayer and in cancer-stem cell-like spheroid culture. The spheroids were generated from adherent breast cancer cells. 6-shogaol was effective in killing both breast cancer monolayer cells and spheroids at doses that were not toxic to noncancerous cells. The percentages of CD44+CD24/low cells and the secondary sphere content were reduced drastically upon treatment with 6-shogaol confirming its action on CSCs. Treatment with 6-shogaol caused cytoplasmic vacuole formation and cleavage of microtubule associated protein Light Chain3 (LC3) in both monolayer and spheroid culture indicating that it induced autophagy. Kinetic analysis of the LC3 expression and a combination treatment with chloroquine revealed that the autophagic flux instigated cell death in 6-shogaol treated breast cancer cells in contrast to the autophagy inhibitor chloroquine. Furthermore, 6-shogaol-induced cell death got suppressed in the presence of chloroquine and a very low level of apoptosis was exhibited even after prolonged treatment of the compound, suggesting that autophagy is the major mode of cell death induced by 6-shogaol in breast cancer cells. 6-shogaol reduced the expression levels of Cleaved Notch1 and its target proteins Hes1 and Cyclin D1 in spheroids, and the reduction was further pronounced in the presence of a γ-secretase inhibitor. Secondary sphere formation in the presence of the inhibitor was also further reduced by 6-shogaol. Together, these results indicate that the inhibitory action of 6-shogaol on spheroid growth and sustainability is conferred through γ-secretase mediated down-regulation of Notch signaling. The efficacy of 6-shogaol in monolayer and cancer stem cell-like spheroids raise hope for its therapeutic benefit in breast cancer treatment.

 

 

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