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Showing posts with label rheumatoid arthritis. Show all posts
Showing posts with label rheumatoid arthritis. Show all posts

Thursday, November 10, 2022

The Epoch Times: Expert Explains Cancer May Be Metabolic Disease, and Shares a Cure : World Health Informatics Blog Cancer

 

The Epoch Times: Expert Explains Cancer May Be Metabolic Disease, and Shares a Cure.

World Health Informatics Blog Cancer

“Cancer is not a genetic disease, it’s a metabolic disease,” Thomas N. Seyfried, a well-known scholar in cancer research and a Professor of Biology at Boston College, told The Epoch Times. “Once people understand that cancer is a metabolic disease, then you will begin to see a very big reduction in death and greatly improved quality of life and survival.”

World Health Informatics Blog Cancer


Cancer Has Remained High for Decades

According to the statistics of the American Cancer Society, although the incidence of cancer in the United States has been declining slowly since the beginning of the 21st century, if we look at it over an extended period of time, we will find that the incidence of cancer is actually increasing, not decreasing.

In 1975, approximately 400 out of every 100,000 Americans had cancer. By 2018, that number had grown to roughly 445, an increase of more than 10 percent [1].

Cancer rates in the United States remain high. (Health 1+1 / The Epoch Times)

From the perspective of cancer mortality, in the past nearly 100 years, the number of women who died of cancer per 100,000 Americans has gradually declined from roughly 190 in 1930 to 130 in 2022; whereas cancer deaths among men per 100,000 Americans rose from around 160 in 1930 to 180 in 2022 [2].

In 2022, nearly 2,000,000 new cancer cases are expected in the United States, and over 500,000 people are expected to die from it. This means that every day, on average, 5,000 Americans are diagnosed with cancer, and over 1,600 people die from it [3].

Cancer May Not Be a Genetic Disease

“Why are so many people dying from cancer?” Seyfried asked. “Because the theory is wrong. The theory that underlies cancer is incorrect.”

Cancer is still generally considered a genetic disorder. Medical textbooks use somatic mutation theory to explain the cause of cancer. These textbooks state that cancer is caused by mutations in proto-oncogenes or tumor suppressor genes [4], and the mutated cells then multiply indefinitely and form malignant tumors. However, Seyfried mentioned a number of facts in this interview and in his published research [5] that are inconsistent with the above theory:

  1. Some cancers do not have genetic and chromosomal mutations;
  2. Some carcinogens do not cause gene mutation;
  3. Cancer “mutations” also occurs in normal cells, but some do not develop further into cancerous cells;
  4. The result of studying cancer as a genetic disorder is the development of personalized treatment or precision medicine, but there are off-target effects for some customized cancer precision medicines.
  5. Ancient people from thousands of years ago rarely had cancer, nor did the indigenous people living in the natural environment.

Seyfried also conducted experiments on nuclear and cytoplasmic transplantation [6], providing evidence for the possibility that cancer is not a genetic disorder.

Under regular circumstances, normal cells develop into normal cells with controlled growth (case 1 in the figure below), while cancer cells develop into cancerous cells with uncontrolled growth (case 2).

Genes are stored in the nucleus. When the nucleus of a cancer cell was implanted into a cytoplasm containing normal mitochondria, the cell developed into a normal cell anyway (case 3). According to the somatic mutation theory, a cell with a cancer cell nucleus should have developed into a cancer cell.

However, when the researchers implanted a normal nucleus into a cancerous cytoplasm with abnormal mitochondria, they found that it still developed into a cancer cell (case 4).

Research suggests that cancer may not be a genetic disorder. (Health 1+1 / The Epoch Times)

Besides, studies of glioma, melanoma, and metastatic breast cancer cells have found that normal mitochondrial function inhibits dysregulated cell growth, regardless of how many genetic or chromosomal abnormalities may be present in the tumor cell nucleus. Seyfried said that all these prove that cell mutation is not the main cause of cancer, and that cancer is in fact, a metabolic disorder.

The Biggest Difference Between Normal Cells and Cancer Cells

The theory that cancer is a metabolic disorder was first proposed about 100 years ago by a well-known German scientist named Otto Warburg. Normal cells break down glucose through aerobic respiration, but Warburg observed that cancer cells are different. Cancer cells obtain energy through fermentation, even in an aerobic environment. Thus, Warburg proposed, aerobic respiratory insufficiency is the origin of cancer.

Seyfried’s research adds another metabolic pathway in cancer cells that Warburg did not observe: cancer cells also get a lot of energy from the fermentation of an amino acid called glutamine, which updated Warburg’s theory [7][8].

The truth, Seyfried said, is that “They [cancer] cannot breathe … they can’t get energy through oxygen, they can only get energy from fermentation.” All cancers can survive without oxygen, but they “cannot live without sugar, glucose, and the amino acid glutamine.”

Cellular aerobic respiration mainly takes place in mitochondria. Mitochondria, which are responsible for respiration, are damaged and hollow in all major types of cancer. The cristae, the wrinkled and wavy structures in the mitochondrial structure, are cluttered and defective. The abnormality of mitochondrial structure will change the function of mitochondria, resulting in the inability of cells to obtain energy through oxidative metabolism. This changes the cell’s metabolism from relying primarily on oxidation to fermentation.

Seyfried further explained that the various abnormalities in cancer cells are caused by the loss of normal function of cell mitochondria due to various reasons (including carcinogens, radiation, pollution, inflammation, age, viruses, etc). A large number of reactive oxygen species (ROS) will be produced when mitochondria are damaged, further attacking and destroying the nucleus.

“The mutations that we see in cancer come as the result of damage from reactive oxygen species,” Seyfried said. “The mutations are an effect, they are not the cause of cancer.”

Defective mitochondrial structure in cancer cells. (Health 1+1 / The Epoch Times)

Furthermore, Seyfried also talked about a phenomenon, that is, cancers with myriad variants share a consistent metastatic process. First, individual cells become cancerous and form tumors; the tumor cells then spread through the blood vessels and circulatory system to other parts of the body, forming new tumors.

Why do all cancers have the same metastatic process? How does this relate to the theory that cancer is a metabolic disorder?

Seyfried said that the mitochondrial metabolic theory explains cancer metastasis better than the somatic mutation theory. After macrophages engulf and fuse with the defective proto-cancer cells, the normally functioning mitochondria are gradually replaced by dysfunctional mitochondria due to inflammation. As immune cells, macrophages have the ability to travel around the body. As a result, these cancer cells, which are fusions of proto-cancer cells and macrophages, spread throughout the body.

Press-Pulse Therapy: Adjust Cancer Cell Metabolism to Improve Condition

Seyfried believes the existing cancer treatment system is “broken.” He said once people understand the metabolic theory of cancer, treatments like chemotherapy and radiotherapy will be replaced by new treatments.

Based on the theory, Seyfried and his team developed the “press-pulse therapy” [9][10][11], which is a cocktail treatment consisting of the ketogenic diet, glutaminase inhibitor medicine, and stress management.

The ketogenic diet is adopted because cancer cells have defective mitochondria and impaired metabolism, so they can only rely on fermented sugars and glutamine for energy. Cancer cells cannot obtain energy as ketone bodies cannot be fermented. As for cells with normal metabolic function, they can obtain energy by metabolizing ketone bodies [12].

The purpose of a ketogenic diet combined with basic drugs is to control the ratio of glucose and ketone bodies in the blood to an ideal range while inhibiting the ability of cancer cells to acquire glutamine. In this way, we can “starve” cancer cells from a metabolic perspective, thereby achieving the same effect as cancer treatments.

An important aspect of “press-pulse therapy” is stress control and emotional management. Seyfried emphasized in the interview that people’s mental stress has a direct relationship with the development of cancer. When patients are diagnosed with cancer, they experience extreme panic and cannot rest or eat in peace. Excessive stress can raise blood sugar levels, which can feed cancer cells into rapid growth. As a result, cancer cannot be controlled. Easing the emotional and stress levels of the patient and his or her family can further stabilize the patient’s psychological and physical condition.

There have been many successful cases of cancer control by managing metabolism. Moreover, many patients use this method when traditional cancer treatments, such as chemotherapy and radiotherapy, are ineffective, or when cancer has spread.

A 38-year-old man developed symptoms in February 2016 and was subsequently diagnosed with glioblastoma multiforme (the most common and malignant form of primary adult brain cancer). After 20 months of ketogenic diet therapy and completion of chemotherapy and radiotherapy, the patient’s tumor decreased by approximately 1.5 cm in diameter. He seemed in good health with no apparent clinical or neurological deficits [13].

Another 54-year-old man was diagnosed with lung cancer; the cancer cells had metastasized and tumors were found in his brain. Radiotherapy and chemotherapy had no effect, so the patient opted for a ketogenic diet. Two years later, the tumors in his brain and lungs shrank; after nine years of treatment, the brain and lung cancer tumors remained stable in size [14].

A 45-year-old woman in Ohio was diagnosed with breast cancer in late 2016. In August 2018, the cancer had spread and she developed tumors in her brain, lungs, mediastinum, liver, abdomen, and bones. Her doctor expected her to have less than a month to live. The patient began receiving press-pulse therapy in November 2018. In April 2019, the scan report indicated that the treatment was effective. According to the published study, her last check-up was in March 2021 and the results showed a stable condition, no recurrence, and improved quality of life [15].

In a study published in the Clinical Nutrition journal, 80 patients with locally advanced and metastatic breast cancer were randomly assigned to a ketogenic diet or a control group for a 12-week treatment test. Patients in the ketogenic diet group had lower serum insulin levels, and their tumors shrank [16].

Two papers recently published in Nature: Prostate Cancer and Prostatic Disease describe the therapeutic benefits of a low-carb diet and a fasting-mimicking diet for patients with prostate cancer [17][18]. A ketogenic diet, which requires fasting and has low carbohydrates, can lower blood sugar levels and control tumor growth. These findings support the hypothesis that elevated ketone bodies are associated with reduced tumor growth [19].

Exercising, Fasting, and Avoiding High-Carb Diets May Keep Cancer Away

World Health Informatics Blog Cancer

As for how an average person can maintain a healthy metabolism and prevent cancer, Seyfried said that by keeping the mitochondria in cells healthy, people are less likely to get cancer. He said this can be achieved through a certain period of fasting (drinking only water), a low-carb diet, and exercise.

He also emphasized that high carbs and unnutritious foods such as junk food can cause cancer, and advised to stay away from such foods. It’s not just cancer, diseases like Alzheimer’s, Type 2 diabetes, and obesity, among others are all related to the Western diet.

“As soon as the Western diet comes into the population, you get cancer … and diabetes and things like this.” He also joked, “The bottom line is don’t eat anything and you’ll get very healthy. Just drink water.”

Flora Zhao

Flora Zhao is a health reporter for The Epoch Times. Have a tip? Email her at: flora.zhao@epochtimes.nyc

 

Thank you

World Health Informatics Blog 

Note :

1) This blog is originally published on 

https://www.theepochtimes.com/health/expert-explains-cancer-may-be-metabolic-disease-and-shares-a-cure_4840835.html?utm_campaign=socialshare_fb&utm_source=facebook.com&fbclid=IwAR2VbdGGc7hXLqjvNWYW-bA2ACYpk6dJJjunJr8qSbJr6PImLBj9dYwYp4M

2) This Blog is for Education purpose only and not a treatment for any diseases  

Tuesday, November 1, 2022

Researchers Discover Anti-inflammatory Molecules That Decline in the Aging Brain - World Health Informatics Blog. (community health)

Researchers Discover Anti-inflammatory Molecules That Decline in the Aging Brain - World Health Informatics Blog. (community health)

Summary: SGDGs, a class of lipids that decline in the brain during aging, appear to have anti-inflammatory effects that could have implications for neurodegenerative disorders.

Source: Salk Institute

World Health Informatics Blog. (community health)

Aging involves complicated plot twists and a large cast of characters: inflammation, stress, metabolism changes, and many others.

Now, a team of Salk Institute and UC San Diego scientists reveal another factor implicated in the aging process—a class of lipids called SGDGs (3-sulfogalactosyl diacylglycerols) that decline in the brain with age and may have anti-inflammatory effects.

The research, published in Nature Chemical Biology on October 20, 2022, helps unravel the molecular basis of brain aging, reveals new mechanisms underlying age-related neurological diseases, and offers future opportunities for therapeutic intervention.

“These SGDGs clearly play an important role in aging, and this finding opens up the possibility that there are other critical aging pathways we’ve been missing,” says co-corresponding author Alan Saghatelian, professor in Salk’s Clayton Foundation Laboratories for Peptide Biology and holder of the Dr. Frederik Paulsen Chair. “This is a pretty clear case of something that should be dug into more in the future.”

SGDGs are a class of lipids, also called fats. Lipids contribute to the structure, development, and function of healthy brains, while badly regulated lipids are linked to aging and diseased brains.

However, lipids, unlike genes and proteins, are not well understood and have often been overlooked in aging research. Saghatelian specializes in discovering new lipids and determining their structures.

His lab, in collaboration with Professor Dionicio Siegel at UC San Diego, made three discoveries involving SGDGs: In the brain, lipid levels are very different in older mice than in younger mice; all SGDG family members and related lipids change significantly with age; and SGDGs may be regulated by processes that are known to regulate aging.

To reach these findings, the team took an unusual, exploratory approach that combined the large-scale study of lipids (lipidomics) with structural chemistry and advanced data analytics.

They first obtained lipid profiles of mouse brains at five ages, ranging from one to 18 months, using liquid chromatography-mass spectrometry. Technological advances in this instrumentation vastly expanded the number of data points available to the scientists, and advanced data analysis allowed them to determine age-related patterns in the enormous lipid profiles.

The team then constructed SGDG molecules and tested them for biological activity.

“SGDGs were first identified in the 1970s, but there were few follow-up studies. These lipids were essentially forgotten and missing from the lipid databases. Nobody knew SGDGs would be changing or regulated in aging, let alone that they have bioactivity and, possibly, be therapeutically targetable,” says first author Dan Tan, a postdoctoral fellow in Saghatelian’s lab at Salk.

The analysis showed that SGDGs possess anti-inflammatory properties, which could have implications for neurodegenerative disorders and other neurological conditions that involve increased inflammation in the brain.

The team also discovered that SGDGs exist in human and primate brains, suggesting that SGDGs may play an important role in animals other than mice. Further research will be required to show if SGDGs contribute to human neuroinflammation.

In the future, the team will examine how SGDGs are regulated with aging and what proteins are responsible for making them and breaking them down, which may open the door to discovering novel genetic activity associated with aging.

“With the understanding of the structure of SGDGs and our ability to create them in the laboratory, the study of these important lipids is now wide open and ripe for discovery,” says Siegel, co-corresponding author of the study.

Additional authors included Meric Erikci Ertunc, Justin Wang, Tina Chang, Antonio F. M. Pinto, Andrea Rocha, Cynthia J. Donaldson, Joan M. Vaughan, Peter C. Gray, Pamela Maher, and Nicola J. Allen of Salk; Srihari Konduri of UC San Diego; Pan Zhang of UC Los Angeles; Raissa G. Ludwig and Marcelo A. Mori of the University of Campinas, Brazil; Elizabeth Willey and Andrew Dillin of UC Berkeley; Manasi Iyer and Bradley Zuchero of Stanford University; and Steven G. Kohama of Oregon Health and Science University.

Funding: This work was funded by Ferring Pharmaceuticals and Frederik Paulsen, the National Institutes of Health (P30 CA014195, R01DK106210, R01NS119823, R01AG069206 and RF1AG061296), the Oregon National Primate Research Center (P51 OD 010092), the Wu Tsai Human Performance Alliance and the Joe and Clara Tsai Foundation, the Anderson Foundation, the Bruce Ford and Anne Smith Bundy Foundation, the Pioneer Fellowship, the Howard Hughes Medical Institute, the CZI Neurodegeneration Network, and The Sãn Paulo Research Foundation (2017/01184-9).

About this aging and neuroscience research news

Author: Salk Communications

Source: Salk Institute

Contact: Salk Communications – Salk Institute

Thank you

World Health Informatics Blog. (community health)

Note :

1) This blog is originally published on 

https://neurosciencenews.com/sgdgs-aging-inflammation-21758/

2) This Blog is for Education purpose only and not a treatment for any diseases  

Image: The image is credited to Salk Institute

Friday, October 28, 2022

Newly discovered species of bacteria in the microbiome may be a culprit behind rheumatoid arthritis World Health Informatics Blog. (community health)

 Newly discovered species of bacteria in the microbiome may be a culprit behind rheumatoid arthritis

World Health Informatics Blog. (community health)

Rheumatoid arthritis affects 1 in 100 people worldwide. It causes inflamed, painful and swollen joints, often in the hands and wrists, and can lead to loss of joint function as well as chronic pain and joint deformities and damage. What causes this condition has been unknown.

World Health Informatics Blog. (community health)

In our recently published study, my colleagues and I found an important clue to a potential culprit behind this disease: the bacteria in your gut.


What causes rheumatoid arthritis?

Rheumatoid arthritis is an autoimmune condition, meaning it develops when the body’s immune system starts to attack itself. Proteins called antibodies, which usually help fight off viruses and bacteria, begin to attack the joints instead.


The origins of the antibodies that cause rheumatoid arthritis have been an area of study for many years. Some research has shown that these antibodies can start forming at sites like the mouth, lung and intestines over 10 years before symptoms arise. But until now, it was unclear why researchers were finding these antibodies in these particular areas.

We wanted to investigate what could trigger the formation of these antibodies. Specifically, we wondered if bacteria in the microbiome, a community of microorganisms that live in the intestines, might be the ones activating the immune response that leads to rheumatoid arthritis. Since microbes commonly live at the same sites as the antibodies driving rheumatoid arthritis, we hypothesized that these bacteria could be triggering the production of these antibodies. We reasoned that though these antibodies were meant to attack the bacteria, rheumatoid arthritis develops when they spread beyond the intestines to attack the joints.


First, we sought to identify the intestinal bacteria targeted by these antibodies. To do this, we exposed the bacteria in the feces of a subset of people at risk for developing rheumatoid arthritis to these antibodies, allowing us to isolate just the bacterial species that reacted and bound to the antibodies.


We found that one previously unknown species of bacteria was present in the intestines of around 20% of people who were either diagnosed with rheumatoid arthritis or produce the antibodies that cause the disease. As a member of the Cherokee Nation of Oklahoma, I suggested we name this species Subdoligranulum didolesgii (“didolesgii” means arthritis or rheumatism in Cherokee) as a nod to the contributions that other Indigenous scholars have made to science as well as the fact that rheumatoid arthritis affects Indigenous people at a higher rate than other populations.


Subdoligranulum didolesgii has not been detected in the feces of healthy people before, and it is currently unknown how prevalent this bacteria is in the general population.


We also found that these bacteria can activate specialized immune cells called T cells in people with rheumatoid arthritis. T cells drive inflammatory responses in the body, and have been linked to the development of different autoimmune diseases.


These findings suggest that these gut bacteria may be activating the immune systems of people with rheumatoid arthritis. But instead of attacking the bacteria, their immune system attacks the joints.


Why this bacteria?

It is still unknown why people with rheumatoid arthritis develop an immune response to Subdoligranulum didolesgii. But we think it may be the culprit when it comes to rheumatoid arthritis because this bacteria is found only in the intestines of people with rheumatoid arthritis, and not in the intestines of healthy people.


While many immune responses happen in the intestines, they are usually self-contained and do not spread to other areas of the body. However, we believe that a particularly strong intestinal immune response against Subdoligranulum didolesgii could allow antibodies to bypass the intestinal “firewall” and spread to the joints.


To confirm our hypothesis, we gave mice an oral dose of Subdoligranulum didolesgii and monitored their reaction. Within 14 days, the mice began to develop joint swelling and antibodies that attacked their joints.


The future of rheumatoid arthritis treatment

My colleagues and I hope this research can shed light on the origins of rheumatoid arthritis. Our next goal is to discover how common these bacteria are in the general population and test whether the presence of these bacteria in the gut may lead to the development of rheumatoid arthritis in people.


It’s important to note that antibiotics are unlikely to be helpful treatment for the microbiomes of patients with rheumatoid arthritis. Although Subdoligranulum didolesgii may be triggering an autoimmune response for some people with rheumatoid arthritis, antibiotics eliminate both helpful and harmful bacteria in the gut. Additionally, removing the bacteria won’t necessarily stop the immune system from attacking the joints once it has started.


Nevertheless, we believe that these bacteria can be used as tools to develop treatments for rheumatoid arthritis and hopefully ways to prevent disease from happening in the first place.


Thank you

World Health Informatics Blog. (community health)

Note :

1) This blog is originally published on 

https://theconversation.com/newly-discovered-species-of-bacteria-in-the-microbiome-may-be-a-culprit-behind-rheumatoid-arthritis-193267

2) This Blog is for Education purpose only and not a treatment for any diseases