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Boron revised

Archives of Toxicology

https://doi.org/10.1007/s00204-018-2296-7

Boric acid and sodium borates are currently classified in the EU-CLP regulation as “toxic to reproduction” under “Category

1B”, with hazard statement of H360FD. However, so far field studies on male reproduction in China and in Turkey could not

confirm such boron-associated toxic effects.

Daily boron intake from the American diet

10.1016/S0002-8223(99)00085-1

As of 1999 the boron intake for American men ranged from 0.46 mg/d to 2.74 mg/d

The role of boron in the functioning of the osteoarticular system

https://doi.org/10.52418/moldovan-med-j.64-5.21.14

UDC: 546.27:616.71/.72

B = boron BCC = boron conaiting compounds

In the past, the poor knowledge of B in the human health conducted that

[65] established a permissible level of B in drinking water of 0.3-0.5 mg B

L-1, this value was so impractical that the European Community (EC) could not meet

with this rule, and changed it to 1.0 mg B L -1, and permitted that their

members countries to adjust it on basis of the quality of its water sources

[66].

According to recently published research, people older

than 40 can prevent/or correct arthritis, osteoporosis and

osteoarthritis by taking B equal to or higher that 3 mg

per day. In the countries following the famous healthy

Mediterranean diet that includes staple foods rich in B such

as grape, broccoli, garlic, tomato, pomegranate and olives

combined with the consumption of drinking water with

high levels of B, daily intake of this trace mineral frequently

results higher than 13 mg per day [8].

Epidemiologic evidence suggests that in the areas of

the world where boron intakes usually were 1 mg or less /

day, the estimated incidence of arthritis ranged from 20 to

70%. On the other hand, in areas of the world where boron

intakes were usually 3 to 10 mg, the estimated incidence of

arthritis ranged from 0 to 10% [10].

Another study has shown that boron levels, along with

those of lead and zinc, were reduced in patients with osteo-

arthritis of the hip when those patients went for hip replace-

ment.

Following the results of a double-blind randomized

placebo-controlled clinical trial with 60 days supplementation

period with calcium fructoborate and sodium tetraborate

for 72 Iraqi patients with active rheumatoid arthritis (RA)

maintained on etanercept, boron as an adjuvant has potenti-

ated therapeutic outcomes in RA patients by improvement

of the clinical scores and significantly decreases the inflam-

matory markers in RA patients [28].

The safety of boron supplements when used in pharma-

cological doses as adjuvant with etanercept in treatment of

RA patients was studied and the results showed that boron

supplements – calcium fructoborate and sodium tetraborate

have no negative impact on erythrocyte sedimentation rate,

hemoglobin, white blood cells, platelets count, hepatic and

renal functions

On average, dried fruits, nuts and avocados contain

between 1 and 4.5 mg of boron/100 g. Fresh fruits, vegetables,

and honey, contains between 0.1 to 0.5 mg boron/100

g, whereas animal foods provide only 0.01 to 0.06 mg of

boron/100 g. Another important source of boron is water,

and the content varies according to geographic location [9].

S0946-672X(18)30156-1

https://doi.org/10.1016/j.jtemb.2018.06.003

B = boron BCC = boron conaiting compounds

It has been known for a long time that B deficiency in soils, leads to depletion of BCCs in fruits and vegetables in the food

supply, was correlated with a high incidence of arthritis [38–40], an inflammatory disease also related to cardiovascular

health [41,42].

Tobacco products contain a plethora of potential toxic molecules, amongst the most cytotoxic of them being nicotine. Diets

enriched in BCCs exhibited a notable risk reduction for cervical cancer, prostate cancer, and also in lung cancer for women

who were heavy smokers [116]. Moreover, the superior natural BCCs intake has been correlated with the most reduced

7lung cancer risks in smoking persons, while the most advanced risk is found in smoking persons with concurrent lack of

hormone replacement therapy (HRT) and low B intake [116].

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Dietary boron supplementation enhances sperm quality and immunity

through influencing the associated biochemical parameters and modulating

the genes expression at testicular tissue

https://doi.org/10.1016/j.jtemb.2019.05.004

Probably the best unitnetional find on boron aside fromt he title. Boron supplementation

led to the increase of Glutathione reductase activity by 3x. Or from 30 mU/ml to 100.

Boron supplementation augmented the immune status in goats as

indicated by the increased level of antioxidant enzyme glutathione re-

ductase in the seminal plasma and catalase in the peripheral blood. The

higher total antioxidant capacity and lower MDA level have been

documented upon boron feeding in rabbits [12].

The adjuvant use of calcium fructoborate and borax with etanercept

in patients with rheumatoid arthritis: Pilot study

DOI:10.5455/jice.20161204021549

Showing major improvement with both sodium tetraborate and calcium

fructoborate

An overview of male reproductive studies of boron with an emphasis on studies

of highly exposed Chinese workers

The study involved male workers at one boron mine and four

boron processing plants in Kuandian City in Liaoning province

in northeast China. The five workplaces were selected based

on the location, number of employees, and the presence and

cooperation of an industrial hygienist at the site. From

the approximately 3500 men in the five workplaces, 957 men

between 18 and 40 years of age agreed to complete an inter-

view to provide demographic, exposure, reproductive, and general

health information.

This series of papers presents an evaluation of a unique group

of boron workers who have biological boron measures higher

than previously reported in humans and is the first study to

include analyses of semen characteristics. There is little detail

on the recruitment of subjects, and therefore, the potential for

selection bias is a concern. With these limitations, however, this

study is reassuring that occupational boron exposure in the range

of 34.4–41.2 mg B/day does not alter sperm count or motility.

Summary Document from the Health Advisory for Boron and Compounds

https://www.epa.gov/sites/default/files/2014-09/documents/summary_document_from_the_ha_for_boron.pdf

Here we have the US government (EPA) listing boron, a vital mineral required for human health and to prevent disease, as a chemical containment

and lying about the dangerous effects it has on human health. I lived in one of the states listed corrupt enough to actually implement these

restrictions and arthritis and osteoporosis was rampant in the elderly population.

How does boron get in my drinking water?

Boron gets into drinking water from both naturally-occurring and man-made

sources. Some areas in the western United States (California, Nevada, Oregon) have high

concentrations of boron in some of their soils. Contamination of water can come directly

from industrial wastewater and municipal sewage, as well as indirectly from air

deposition and soil runoff. Natural weathering processes, burning of coal in power

plants, chemical plants, and manufacturing facilities releases boron into the air; and

fertilizers, herbicides, and industrial wastes are among the sources of soil contamination.

How will I know if I have boron in my drinking water?

The Federal Government does not regulate boron in drinking water and, public

drinking water systems are not required to monitor for this contaminant. Some states have

drinking water standards or guidelines for boron (California, Florida, Maine, Minnesota,

New Hampshire and Wisconsin); these range from 0.6 to 1 mg/L. You may want to call

your drinking water utility or state drinking water program to determine if monitoring is

required in your state.

Boron inhibits the proliferating cell nuclear antigen index, molybdenum

containing proteins and ameliorates oxidative stress in hepatocellular carcinoma

dx.doi.org/10.1016/j.abb.2012.11.008

>>22691366

Millions have died supposedly and I haven't seen a single video involving any mass casualties. Those telegram channel have like nothing on them.

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Duchenne muscular dystrophy (DMD)

The primary mechanism for DMD seems to be the dysfunction of glycolysis pathway, or processing glucose for energy.

Of note, the study uses a modified ketogenic diet that has a higher amount of carbs. Any human

eating the percentage of carbs they used in this study would not be in full ketosis, if at all. A lower carb diet

might show even better results.

Ketogenic diet with medium-­chain triglycerides restores

skeletal muscle function and pathology in a rat model of

Duchenne muscular dystrophy

https://doi.org/10.1096/fj.202100629R

MCT-KD: ketogenic diet supplemented with medium

chain triglycerides.

ND, normal diet

WT, Wild type rat

3.1 | KD with MCT causes continuous

ketosis without loss of body weight in

DMD rats

We evaluated the effects of feeding DMD rats with either

an MCT- KD or an ND between the ages of 3 and 12 weeks.

The ketogenic ratio of fat to the carbohydrate-plus- protein

weight of the MCT- KD was 1.95 for the first 10 days and

1.43 for the remainder of the study (Table 1). The ND

group was pair- fed with MCT-KD based on daily caloric

intake, because KD decreases appetite and food intake in

mice and rats.28

Figure 1A shows that BW did not significantly dif-

fer between the ND and MCT-KD DMD rats. By the age

of 12 weeks, the BW of these rats was ~83% of that of

DMD rats fed ad libitum (data not shown). At the age of

10 weeks, concentrations of postprandial blood glucose

were significantly higher in the ND, than the MCT-KD

rats, although their fasting blood glucose values were

identical (Figure 1B). Postprandial concentrations

of blood ketone bodies were significantly higher in

MCT-KD, than in ND rats, but identical between them

under fasting conditions (Figure 1C). Blood concentra-

tions of glucose and ketone bodies were identical be-

tween fasting and postprandial MCT-KD rats, and like

those of fasting ND rats.

3.2 | Skeletal muscle dysfunction is

suppressed by the MCT-KD in DMD rats

Grip strength at the age of 12 weeks was 21.4% higher in

MCT-KD, compared with ND rats (Figures 2A and S1A).

The relative TA muscle weight to BW was increased by

16.2% in MCT-KD, compared with ND rats, although the

weight of soleus muscle did not significantly differ be-

tween the groups (Figures 2B,C and S1B,C). The relative

weight of eWAT to BW was slightly, but not significantly

decreased by MCT-KD (Figures 2D and S1D). We evalu-

ated the effects of MCT-KD on skeletal muscle pathology

by staining the TA muscles of DMD rats with hematoxy-

lin and eosin (HE; Figure 2E). The MCT-KD obviously

suppressed the appearance of small skeletal muscle fib-

ers that were evident in ND rats. The distribution of the

minimal Feret diameter of muscle fibers showed that

MCT-KD increased the size of muscle fibers in the DMD

rats (Figure 2F).

3.3 | Muscle necrosis, inflammatory cell

infiltration, and fibrosis are suppressed by

MCT- KD in DMD rats

Immunohistochemical analysis of IgG and albumin

in sections of TA muscles from DMD rats showed that

MCT-KD significantly suppressed the increase in IgG and

albumin uptake, a marker of damage to muscle cell mem-

branes29,30 (Figures 3A,B and S2A,B). This was in accord-

ance with the decline in serum CK activity in MCT-KD

rats (Figure 3C). The number of CD11b positive cells, a

marker of monocytes, was significantly decreased, in-

dicating that skeletal muscle damage was suppressed

(Figure 3D,E). The ratio of Foxp3 + CD25 + cells, a marker

of immunosuppressive regulatory T cells (Tregs), to

CD4 + CD11b − cells that are associated with the suppres-

sion of muscular damage, 31 was significantly higher in

the MCT-KD, than ND rats (Figure 3F). The mRNA ex-

pression of TGF-β1 , which regulates extracellular matrix

(ECM) remodeling, was significantly decreased by the

MCT-KD (Figure 3G). Masson trichrome staining showed

that the MCT-KD significantly suppressed DMD-induced

fibrosis (Figure 3H,I).

>>22691541

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3.4 | Proliferation of satellite stem cells

is promoted by MCT-KD

We investigated the effects of MCT-KD on muscle regen-

eration in the DMD rats. Immunohistochemical analysis

of eMHC, a marker of regenerated myofibers, showed that

the DMD rats fed with MCT-KD tended to have fewer

eMHC+ myofibers (Figure 4A,B). Ratios of fibers with

central nuclei did not significantly differ between DMD

rats fed with the MCT- KD and ND (Figure S2A). We im-

munohistochemically assessed the SC markers, Pax7 and

MyoD, in sections of TA muscle from ND and MCT-KD

rats (Figure 4C–G). We also examined the proliferative

potential of SCs by double staining with Ki67 and Pax7 or

MyoD. The number of Pax7 + and MyoD + cells tended to

decrease in the MCT- KD rats. The ratios of Ki67 + Pax7 +

cells to Pax7 + cells and Ki67 + MyoD + cells to MyoD + cells

were significantly increased in the MCT-KD rats. The

mRNA expression of FGF2, which promotes the prolifera-

tion of muscle SCs, was significantly increased in the TA

muscles of MCT-KD rats (Figure 4H).

3.5 | MCT- KD suppressed DMD

progression for 9 months

We investigated the long- term effects of MCT-KD on

DMD. The DMD rats were fed with either the MCT-KD

or the ND for 33 weeks from 3 weeks of age (Figure 5A,B).

The reference was WT siblings of DMD rats fed with the

ND. All rats were given food ad libitum and maintained

in groups of 2– 4 per cage. One DMD rat each fed with

MCT-KD and ND died due to DMD at 4 months of age,

but all other rats remained alive at 9 months of age.

The grip strength findings showed stronger muscles

in the MCT-KD, than the ND DMD rats at the ages of 5,

7, and 9 months (Figures 5B and S3A), and the MCT-KD

rats at the age of 7 months were as strong as they were at

the age of 4 months, whereas the ND-treated DMD rats

lost muscle strength with age. The muscle strength of

the MCT-KD rats at the age of 7 months did not signifi-

cantly differ from that of WT rats fed with the ND. Unlike

at 3 months of age, the TA, soleus muscle, and adipose

tissue weight did not significantly differ between ND

and MCT-KD (Figure S3B–F). We evaluated the effects

of MCT-KD on skeletal muscle pathology by staining TA

muscles with HE (Figure 5C). The MCT-KD suppressed

the appearance of small skeletal muscle fibers that was

evident in ND rats. The distribution of the minimal Feret

diameter of muscle fibers showed that MCT-KD increased

the size of muscle fibers in the DMD rats (Figure 5D), and

Masson trichrome staining showed that MCT-KD signifi-

cantly suppressed DMD-induced fibrosis (Figure 5E,F).

Serum CK activity did not significantly differ between the

ND and MCT-KD groups (Figure S3H)

>>22691579

Antipasto

>>22691635

When do they get to schumann? I thought 5th grade science was for men having periods and women having penis'.

>>22691394

Wow you're stupid. The children are disposed of eventually and they have to go somewhere. 300,000 children go missing every year, I think those were the stats. At an average weight of 80 pounds that's 24 million pounds.

>>22691653

He has one of those words of wisdom calendars. Cherish it, we'll have to wait a month for the next one.

>>22691669

You're so disconnected from reality. The system bogs you down with so much worthless busy work that you don't have time to educate yourself properly. Why do you think so many people were asleep?