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This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
For the great majority of people, the major factor that increases a person's risk for colorectal cancer (CRC) is increasing age. Risk increases dramatically after age 50 years; 90% of all CRCs are diagnosed after this age. The history of CRC in a first-degree relative, especially if before the age of 55 years, roughly doubles the risk. Other risk factors are weaker than age and family history. People with inflammatory bowel disease have a much higher risk of CRC. A small percentage (<5%) of CRCs occur in people with a genetic predisposition, including familial adenomatous polyposis and hereditary nonpolyposis coli.
Note: Separate PDQ summaries on Colorectal Cancer Screening; Colon Cancer Treatment; and Rectal Cancer Treatment are also available.
Factors Associated With Increased Risk of Colorectal Cancer
Excessive alcohol use
Based on solid evidence from observational studies, excessive alcohol use is associated with an increased risk of colorectal cancer (CRC).[1,2,3]
Magnitude of Effect: A pooled analysis of eight cohort studies estimated an adjusted relative risk (RR) of 1.41 (95% confidence interval [CI], 1.16–1.72) for consumption exceeding 45 g/day.
Cigarette smoking
Based on solid evidence, cigarette smoking is associated with increased incidence and mortality from CRC.
Magnitude of Effect: A pooled analysis of 106 observational studies estimated an adjusted RR (current smokers vs. never smokers) for developing CRC of 1.18 (95% CI, 1.11–1.25).
Based on solid evidence, obesity is associated with increased incidence and mortality from CRC.
Magnitude of Effect: In one large cohort study, the adjusted RR for developing colon cancer for women with a body mass index of more than 29 was 1.45 (95% CI, 1.02–2.07). A similar increase in CRC mortality was found in another large cohort study.
Factors Associated With a Decreased Risk of Colorectal Cancer
Physical activity
Based on solid evidence, regular physical activity is associated with a decreased incidence of CRC.
Magnitude of Effect: A meta-analysis of 52 observational studies found a statistically significant 24% reduction in CRC incidence (RR = 0.76; 95% CI, 0.72–0.81).
Interventions Associated With Decreased Risk of Colorectal Cancer
Nonsteroidal anti-inflammatory drugs
There is inadequate evidence that the use of nonsteroidal anti-inflammatory drugs (NSAIDs) reduces the risk of CRC. In people without genetic predisposition but with a prior history of a colonic adenoma that had been removed, three randomized controlled trials (RCT) found that celecoxib [9,10] and rofecoxib [11] decrease the incidence of recurrent adenoma, although follow-up was too short to determine whether the incidence of CRC would have been affected.
Based on solid evidence, NSAIDs reduce the risk of adenomas, but the extent to which this translates into a reduction of CRC is uncertain.
Based on solid evidence, harms of NSAID use are relatively common and potentially serious, and include upper gastrointestinal bleeding, chronic kidney disease, and serious cardiovascular events such as myocardial infarction, heart failure, and hemorrhagic stroke.[12]
Magnitude of Effect: The estimated average excess risk of upper gastrointestinal complications in average-risk people attributable to NSAIDs is 4/1,000 to 5/1,000 people per year. The excess risk varies with the underlying gastrointestinal risk, however, it likely exceeds ten extra cases per 1,000 people per year in more than 10% of users. Serious cardiovascular events are increased by 50% to 60%.
Based on solid evidence, daily aspirin (acetylsalicylic acid [ASA]) for at least 5 years reduces CRC incidence and mortality. This is based on two reports of extended follow-up of two RCTs [16,17] and meta-analysis of observational studies.[16] A third report that adds extended follow-up of an additional two RCTs (with a meta-analysis of all four RCTs) adds certainty to this conclusion.[18]
Magnitude of Effect: After 23 years of follow-up, incidence of CRC in the placebo group was 3.8% and in the ASA group 2.5% (hazard ratio [HR] = 0.63; 95% CI, 0.47–0.85). In the report from all four RCTs, the 20-year risk of death due to CRC in trials that allocated ASA for at least 5 years was reduced by about 40% (HR = 0.60; 95% CI, 0.45–0.81), absolute risk reduction was from about 3.1% to 1.9%. The primary effect was on mortality from proximal colon cancer.
Based on solid evidence, harms of ASA use include excessive bleeding, including gastrointestinal bleeds and hemorrhagic stroke.
Magnitude of Effect: The estimated average excess risk of upper gastrointestinal complications is 10 to 30 per 1,000 people for a period of 10 years, on the higher end for men and on the lower end for women. Risk increases with age.
Postmenopausal hormones
Based on solid evidence, postmenopausal estrogen plus progesterone hormone use, but not estrogen alone, decreases the incidence of CRC.[21]
Magnitude of Effect: In the Women's Health Initiative (WHI), there was a 44% reduction in CRC incidence in the estrogen and progesterone group but not in the estrogen-only group. The absolute reduction in the incidence of CRC was 0.6 cancers per 1,000 women, from 1.6 cancers per 1,000 women to 1.0 cancer per 1,000 women. A meta-analysis of 18 observational studies showed a 20% reduction in colon cancer incidence among women who had ever used hormone therapy (RR = 0.80; 95% CI, 0.74–0.86) compared with nonusers and a 34% reduction among current users (RR = 0.66; 95% CI, 0.59–0.74).
Based on solid evidence, harms of postmenopausal combined estrogen plus progestin hormone use include increased risk of breast cancer, coronary heart disease, and thromboembolic events.
Magnitude of Effect: The WHI showed a 26% increase in invasive breast cancer in the combined hormone group, a 29% increase in coronary heart disease events, a 41% increase in stroke rates, and a twofold higher rate of thromboembolic events.
Polyp removal
Based on fair evidence, removal of adenomatous polyps reduces the risk of CRC. Much of this reduction likely comes from removal of large (i.e., >1.0 cm) polyps, while the benefit of removing smaller polyps—which are much more common—is unknown. Some but not all observational evidence indicates that this reduction may be greater for left-sided CRC than for right-sided CRC.[24,25,26]
Magnitude of Effect: Unknown, probably greater for larger polyps (i.e., >1.0 cm) than smaller ones.
Based on solid evidence, the major harms of polyp removal include perforation of the colon and bleeding.
Magnitude of Effect: Seven to nine events per 1,000 procedures.
Diet modification
A diet low in fat and meat and high in fiber, fruits, and vegetables
Based on fair evidence, a diet low in fat and meat and high in fiber, fruits, and vegetables started as an adult does not reduce the risk of CRC by a clinically important degree.
There are no known harms from dietary modification, including reduction of fatty acids or meats and an increase in the intake of fiber, fruits, and vegetables.
Calcium supplementation
The evidence is inadequate to determine whether calcium supplementation reduces the risk of CRC.
The evidence is fair that elemental calcium without vitamin D as a supplement in the level of 1,000 to 1,200 mg/day increases the risk of myocardial infarction. Based on fair evidence, calcium supplementation with vitamin D at doses less than 1,000 has few harms.
Magnitude of Effect: In a meta-analysis of RCTs of calcium alone, the risk of myocardial infarction was increased from 4.8% to 5.8% (HR = 1.31; 95% CI, 1.02–1.67).
Based on solid evidence, statins do not reduce the incidence or mortality from CRC.
Based on solid evidence, the harms of statins are small.
Incidence and mortality
Colorectal cancer (CRC) is the third most common malignant neoplasm worldwide [1] and the second leading cause of cancer deaths (irrespective of gender) in the United States.[2] It is estimated that there will be 143,460 new cases diagnosed in the United States in 2012 and 51,690 deaths due to this disease.[2] Between 2004 and 2008, CRC incidence rates in the United States declined by 2.5% per year in women, and by 2.7% per year in men.[2] For the past 20 years, the mortality rate has been declining. There was a 1.8% decline in mortality rate per year between 1985 and 2002. Between 2002 and 2005, the mortality rate declined by 4.3% per year. However, in adults younger than 50 years, CRC incidence rates have been increasing by about 1.7% per year since 1992 in men and women.[2] The overall 5-year survival rate is 64%. About 5% of Americans are expected to develop the disease within their lifetimes.[2,3] The risk of CRC begins to increase after the age of 40 years and rises sharply at ages 50 to 55 years; the risk doubles with each succeeding decade, and continues to rise exponentially. Despite advances in surgical techniques and adjuvant therapy, there has been only a modest improvement in survival for patients who present with advanced neoplasms.[4,5] Hence, effective primary and secondary preventive approaches must be developed to reduce the morbidity and mortality from CRC.
Definition of prevention
Primary prevention involves the use of medications or other interventions before the clinical appearance of CRC with the intent of preventing clinical CRC and CRC mortality.
Etiology and pathogenesis of colorectal cancer
Genetics,[6,7] experimental,[8,9] and epidemiologic [10,11,12] studies suggest that CRC results from complex interactions between inherited susceptibility and environmental factors. The exact nature and contribution of these factors to CRC incidence and mortality is the subject of ongoing research.
Factors associated with increased risk of colorectal cancer
There is evidence of an association of CRC with alcoholic beverage consumption. In a meta-analysis of eight cohort studies, the relative risk (RR) for consumption of 45 g/day (i.e., about three standard drinks/day) compared with nondrinkers was 1.41 (95% confidence interval [CI], 1.16–1.72).[13] Case-control studies suggest a modest-to-strong positive relationship between alcohol consumption and large bowel cancers.[14,15] A meta-analysis found that the association did not vary by sex or location within the large bowel.[16]
Five studies have reported a positive association between alcohol intake and colorectal adenomas.[17] A case-control study of diet, genetic factors, and the adenoma-carcinoma sequence was conducted in Burgundy.[18] It separated adenomas smaller than 10.0 mm in diameter from larger adenomas. A positive association between current alcohol intake and adenomas was found to be limited to the larger adenomas, suggesting that alcohol intake could act at the promotional phase of the adenoma-carcinoma sequence.[18]
A large cohort study found a dose-response relationship between alcohol intake and death from CRC, with a RR of 1.2 (95% CI, 1.0–1.5) for four or more drinks per day compared with nondrinkers.[19]
Most case-control studies of cigarette exposure and adenomas have found an elevated risk for smokers.[20] In addition, a significantly increased risk of adenoma recurrence following polypectomy has been associated with smoking in both men and women.[20] In the Nurses' Health Study, the minimum induction period for cancer appears to be at least 35 years.[21] Similarly, in the Health Professionals Follow-up Study, a history of smoking was associated with both small and large adenomas and with a long induction period of at least 35 years for CRC.[22] In the Cancer Prevention Study II (CPS II), a large nationwide cohort study, multivariate-adjusted CRC mortality rates were highest among current smokers, intermediate among former smokers, and lowest in nonsmokers, with increased risk observed after 20 or more years of smoking in men and women combined.[23] On the basis of CPS II data, it was estimated that 12% of CRC deaths in the U.S. population in 1997 were attributable to smoking. A large population-based cohort study of Swedish twins found that heavy smoking of 35 or more years' duration was associated with a nearly threefold increased risk of developing colon cancer, though subsite analysis found a statistically significant effect only for rectal but not colon cancer.[24] Another large population-based case-control study supports the view that current tobacco use and tobacco use within the last 10 years is associated with colon cancer. A 50% increase in risk was associated with smoking more than a pack a day relative to never smoking.[25] However, a 28-year follow-up of 57,000 Finns showed no association between the development of CRC and baseline smoking status, though there was a 57% to 71% increased risk in persistent smokers.[26] No relationship was found between cigarette smoking, even smoking of long duration, and recurrence of adenomas in a population followed for 4 years after initial colonoscopy.[27]
A meta-analysis of 106 observational studies found a RR (ever smokers compared with nonsmokers) for CRC incidence of 1.18 (95% CI, 1.11–1.25), with an absolute risk increase of 10.8 cases per 100,000 person-years (95% CI, 7.9–13.6). There was a statistically significant dose-response effect. In 17 studies with data on CRC mortality, cigarette smoking was associated with CRC death, with a RR (ever smokers vs. never smokers) of 1.25 (95% CI, 1.14–1.37), and an absolute increase in the death rate of 6.0 deaths per 100,000 person-years. For both incidence and mortality, the association was stronger for rectal cancer than for colon cancer.[28]
At least three large cohort studies have found an association between obesity and CRC incidence or mortality.[29,30,31] The Nurses' Health Study found that women with a body mass index (BMI) of more than 29, compared with women with a BMI of less than 21, had an adjusted RR for CRC incidence of 1.45 (95% CI ,1.02–2.07).[29] In the CPS II [31], men and women with a BMI of 30 to 34.9 had an adjusted RR for CRC mortality (compared with people with a BMI of 18.5–24.9) of 1.47 (95% CI, 1.30–1.66), with a statistically significant dose-response effect.[31] The effects were similar in men and women.
Factors associated with a decreased risk of colorectal cancer
A sedentary lifestyle has been associated in some [32,33] but not all [34] studies with an increased risk of CRC. Numerous observational studies that have examined the relationship between physical activity and colon cancer risk.[35] Most of these studies have shown an inverse relationship between level of physical activity and colon cancer incidence. The average RR reduction is reportedly 40% to 50%. Large U.S. cohort studies have found statistically significant adjusted RR of 0.54 (95% CI, 0.33–0.90) [29] and 0.53 (95% CI, 0.32–0.88) [30] when comparing people with high versus low average energy expenditure. A meta-analysis of 52 observational studies found an overall adjusted RR of 0.76 (95% CI, 0.72–0.81), with similar results for men and women.[36]
Interventions associated with a decreased risk of colorectal cancer: Benefits and harms
One large cohort study (301,240 people with 3,894 colorectal cancer cases) found an association between daily or weekly nonaspirin (non–acetylsalicylic acid [non-ASA]) nonsteroidal anti-inflammatory drug (NSAID) use and reduced 10-year incidence of proximal and distal colon cancer, but not rectal cancer, with a hazard ratio (HR) of 0.67 (95% CI, 0.58–0.77) for daily use for colon cancer. Because exposure to non-ASA NSAIDs was assessed only once, assessment was by self-report, and there is no information on dose or duration of use, the certainty of this single study must be rated low. Further research is needed before this finding can be accepted.[37]
Although evidence is currently inadequate to determine whether NSAIDs reduce CRC incidence, proponents suggest that any effect of these drugs results from their ability to inhibit the activity of cyclooxygenase (COX). COX is important in the transformation of arachidonic acid into prostanoids, prostaglandins, and thromboxane A2. NSAIDs include not only aspirin (acetylsalicylic acid [ASA]) (which is considered separately here) and other, first-generation nonselective inhibitors of the two functional isoforms of COX, termed COX-1 and COX-2, but also newer second-generation drugs that inhibit primarily COX-2. Normally, COX-1 is expressed in most tissues and primarily plays a housekeeping role (e.g., gastrointestinal mucosal protection and platelet aggregation). COX-2 activity is crucial in stress responses and in mediating and propagating the pain and inflammation that are characteristic of arthritis.[38]
Nonselective COX inhibitors include indomethacin (Indocin); sulindac (Clinoril); piroxicam (Feldene); diflunisal (Dolobid); ibuprofen (Advil, Motrin); ketoprofen (Orudis); naproxen (Naprosyn); and naproxen sodium (Aleve, Anaprox). Selective COX-2 inhibitors include celecoxib (Celebrex), rofecoxib (Vioxx), and valdecoxib (Bextra). Rofecoxib and valdecoxib are no longer marketed because of an associated increased risk of serious cardiovascular events.
Both celecoxib and rofecoxib have been associated with serious cardiovascular events including dose-related death from cardiovascular causes, myocardial infarction, stroke, or heart failure.[39,40,41,42] Four trials that demonstrated this increased risk are summarized in the Table. In addition, a network meta-analysis of all large scale (RCTs) comparing any NSAID to any other NSAID or placebo found that there is little evidence to suggest that any of the investigated drugs are safe in cardiovascular terms. Naproxen seemed least harmful.[43]
Other major harms from all NSAIDs are gastrointestinal bleeding and renal impairment. The incidence of reported major gastrointestinal bleeding events appears to be dose-related.[44]
Celecoxib reduces the incidence of adenomas; however, celecoxib does not have a clinical role in reducing the risk of sporadic CRC. Its long-term efficacy in preventing CRC has not been shown due to increased risk of cardiovascular events, and because there are other effective ways, such as screening to reduce CRC mortality.[45] A population-based retrospective cohort study of nonaspirin NSAID use among individuals aged 65 years and older was associated with lower risk of CRC, particularly with longer durations of use.[46]
Several studies conducted in a rigorous manner have demonstrated the effectiveness of sulindac in reducing the size and number of adenomas in familial polyposis.[47,48] In a randomized, double-blind, placebo-controlled study of 77 patients with familial adenomatous polyposis, patients receiving 400 mg of celecoxib twice a day had a 28.0% reduction in the mean number of colorectal adenomas (P = .003 for the comparison with placebo) and a 30.7% reduction in the polyp burden (sum of polyp diameters; P = .001) as compared with reductions of 4.5% and 4.9%, respectively, in the placebo group. The reductions in the group receiving 100 mg of celecoxib twice a day were 11.9% (P = .33 for the comparison with placebo) and 14.6% (P = .09), respectively. The incidence of adverse events was similar among the groups.[49]
The NSAID piroxicam, at a dose of 20 mg/day, reduced mean rectal prostaglandin concentration by 50% in individuals with a history of adenomas.[50] Several studies assessing the effect of ASA or other nonsteroidals on polyp recurrence following polypectomy are in progress.[51] In several of these studies, mucosal prostaglandin concentration is being measured.
The potential for the use of NSAIDs as a primary prevention measure is being studied. There are, however, several unresolved issues that mitigate against making general recommendations for their use. These include a paucity of knowledge about the proper dose and duration for these agents, and concern about whether the potential preventive benefits such as a reduction in the frequency or intensity of screening or surveillance could counterbalance long-term risks such as gastrointestinal ulceration and hemorrhagic stroke for the average-risk individual.[52]
The preponderance of evidence from both observational studies and long-term follow-up of RCTs indicates that daily ASA for at least 5 years reduces the incidence of CRC. Among a group of more than 600,000 adults enrolled in an American Cancer Society study, mortality in regular users of ASA was about 40% lower for cancers of the colon and rectum.[53,54] In a report from the Health Professionals Follow-up Study of 47,000 males, regular use of ASA (at least 2 times per week) was associated with a 30% overall reduction in CRC, including a 50% reduction in advanced cases.[55] In a Women's Health Study of a randomized 2 x 2 factorial trial of 100 mg of ASA every other day for an average of 10 years, similar rates of breast, colorectal, or other site-specific cancers were observed in both the ASA and placebo arms.[56] In a report from the Nurses' Health Study involving 82,911 women followed for 20 years, the multivariate RR for colon cancer was 0.77 (95% CI, 0.67–0.88) among women who regularly used ASA (≥2 standard 325-mg tablets per week) compared with nonregular use. Significant RR was not observed, however, until more than 10 years of use. The benefit appeared to be dose-related (e.g., women who used more than 14 ASA per week for longer than 10 years had a multivariate RR for cancer of 0.47 [95% CI, 0.31–0.71]).
A systematic review of 46 observational studies of ASA and CRC in 2007 found a reduction in CRC (OR for any use 0.80 [0.73–0.87]).[57] A large cohort study (301,240 people with 3,894 colorectal cancer cases) published after this systematic review found an association between weekly or daily ASA use and reduced 10-year incidence of distal and rectal (but not proximal) colorectal cancer, with an HR of 0.76 (95% CI, 0.64–0.90) for rectal cancer for daily use. However, use was assessed at only one time, and there is no information about dose or duration of use.[37]
In the Physicians' Health Study, 22,000 men aged 40 to 84 years were randomly assigned to receive placebo or ASA (325 mg every other day) for 5 years. There was no reduction in invasive cancers or adenomas at a median follow-up of 4.5 years.[58] In a subsequent analysis of more than 12 years, both randomized and observational analyses indicated that there was no association between the use of ASA and the incidence of CRC. The low dose of ASA and the short treatment period may account for the null findings.[59]
In a randomized study of 635 patients with prior CRC (T1–T2 N0 M0) who had undergone curative resection, ASA intake at 325 mg/day was associated with a decrease in the adjusted RR of any recurrent adenoma as compared with the placebo group (0.65; 95% CI, 0.46–0.91) after a median duration of treatment of 31 months. The time to detection of a first adenoma was longer in the ASA group than in the placebo group (HR for the detection of a new polyp, 0.54; 95% CI, 0.43–0.94, P = .022). Harms of treatment included upper gastrointestinal hemorrhage and hemorrhagic stroke.[60] In a study of 1,121 patients with a recent history of colorectal adenomas, after a mean duration of treatment of 33 months, the unadjusted RRs of any adenoma (as compared with the placebo group) were 0.81 in the 81-mg ASA group (95% CI, 0.69–0.96) and 0.96 in the 325-mg ASA group (95% CI, 0.81–1.13). For advanced neoplasms (adenomas measuring at least 10.0 mm in diameter or with tubulovillous or villous features, severe dysplasia, or invasive cancer), the RRs were 0.59 (95% CI, 0.38–0.92) in the 81-mg ASA group, and 0.83 (95% CI, 0.55–1.23) in the 325-mg ASA group.[61] Harms of treatment were similar in the two groups and included upper gastrointestinal bleeding and hemorrhagic stroke.
Four reports in 2007, 2010, 2011, and 2012 [57,62,63,64] have analyzed long-term follow-up of RCTs of daily ASA versus the control. The 2007 analysis reported on two RCTs with reliable follow-up of more than 20 years. This report found that the use of 300 mg or more of ASA per day for at least 5 years reduced the incidence of CRC after a latency of 10 years (RR at 10–19 years [0.60; 95% CI, 0.42-0.87]). The 2010 analysis analyzed long-term follow-up data from four RCTs, finding that allocation to ASA for 5 or more years reduced the 20-year incidence and mortality of proximal colon cancer (adjusted incidence HR = 0.35; 95% CI, 0.20–0.63; adjusted mortality HR = 0.24; 95% CI, 0.11–0.52) and also reduced the 20-year risk of rectal cancer (RR = 0.58; 95% CI, 0.36–0.92) but not distal colon cancer. There was no increase in benefit at doses more than 75 mg/day. The absolute 20-year risk reduction in fatal CRC was 1.76% (95% CI, 0.61–2.91).
The 2011 analysis examined data from eight RCTs, seven of which provided individual patient data and three of which provided 20-year follow-up data. In trials with allocation to ASA of at least 5 years, the 20-year HR for CRC mortality was 0.60 (95% CI, 0.45–0.81). Six RCTs, including five from the United Kingdom, were included in a meta-analysis in which patients were randomly assigned to receive either aspirin or placebo and mean scheduled duration of trial treatment was 4 years or more. Individual patient data for all in-trial cancer deaths were obtained. In the three United Kingdom trials, cancer deaths after completion of the trials were obtained via death certification and cancer registration, taking the follow-up to 20 years after randomization. Based on meta-analysis of odds ratios from each trial rather than on more sensitive actuarial analysis of the individual patient data, allocation to aspirin in the RCTs reduced the 20-year risk of death due to colorectal (and esophageal) cancer. Odds ratios for 'maximum aspirin use' were 0.55 for colorectal cancer risk (95% CI, 0.41–0.76) and 0.47 for esophageal cancer risk (95% CI, 0.27–0.81) and for 'any aspirin use' were 0.58 for colorectal cancer risk (95% CI, 0.44–0.78) and 0.51 for esophageal cancer (95% CI, 0.31–0.83).
In a large cohort study, an association between recent daily aspirin use and lower-cancer mortality in the gastrointestinal tract (RR = 0.61; 95% CI, 0.47–0.78), liver (RR = 0.52; 95% CI, 0.30–0.93), and bladder (RR = 0.52; 95% CI, 0.28–0.97) were observed among the 100,139 analysis-eligible participants from the Cancer Prevention Study II Nutrition Cohort established by the American Cancer Society in 1982. The analysis excluded participants who had a history of cancer in the baseline year or whose records contained incomplete information on aspirin use or smoking, and was based on follow-up questionnaires mailed to participants in 1997 (the baseline year for the analysis), 1999, 2001, and 2003. Mortality follow-up continued through Dec 31, 2008 via automated linkage to the National Death Index vital status and cause of death codes (ICD-10); death certificates were obtained for 99.3% of known deaths.[65]
Postmenopausal female hormone supplements
Several observational studies have suggested a decreased risk of colon cancer among users of postmenopausal female hormone supplements.[66,67,68,69] For rectal cancer, most studies have observed no association or a slightly elevated risk.[70,71,72]
In the Women's Health Initiative (WHI) Trial, 16,608 postmenopausal women aged 50 to 79 years were randomly assigned to a combination of conjugated equine estrogens (0.625 mg/day) plus medroxyprogesterone (2.5 mg/day) or placebo. There were 43 invasive CRCs in the hormone group and 72 in the placebo group (HR = 0.56; 95% CI, 0.38–0.81; P = .003). The invasive CRCs in the hormone group were similar in histologic features and grade to those in the placebo group but with a greater number of positive lymph nodes (mean ± standard deviation 3.24 ± 4.1 vs. 0.8 ± 1.7; P = .002) and were more advanced (regional or metastatic disease; 76.2% vs. 48.5%; P = .004).[73]
An analysis of data from the National Polyp Study (NPS), with external, historical controls, has commonly been cited to show a reduction of 76% to 90% in the subsequent incidence of CRC after colonoscopic polypectomy compared with three nonconcurrent, historical control groups.[74] This study may be biased in several ways that inflate the apparent efficacy of polyp removal; the main problem is that potential enrollees in the National Polyp Study were excluded if they had CRC at their baseline examination. Because no such exclusions (or baseline colonoscopy examinations) were done in the three comparison groups, persons who had CRC at baseline would be counted as having incident CRC in subsequent follow-up. Although adjustments were attempted, it is not possible to know the magnitude of the impact of this problem on the result because it is not known how long CRC may be present without causing symptoms.
A long-term follow-up study (median follow-up period, 15.8 years; maximum, 23 years) of the NPS cohort suggested an approximately 53% reduction in CRC mortality due to polypectomy (not just exclusion of persons with CRC at initial exam). However, the degree of reduction must be viewed with caution because this study did not have a direct comparison group, relying mainly on comparison to expected data from the Surveillance, Epidemiology and End Results Program. Further, details are not clear about exactly what the program of colonoscopy was that may have led to decreased mortality. Patients in the NPS were assigned to colonoscopy at years 1 and 3; colonoscopy was also offered to one of the two comparison groups at year 1; all participants were offered colonoscopy at year 6. However, following year 6, the exact surveillance that patients may have undergone and how that surveillance might have been associated with decreased CRC mortality were not clear. [75]
It is expected that further follow-up in the United Kingdom Flexible Sigmoidoscopy Screening Trial will be able to provide more detail about the long-term effect of polypectomy, at least on the left side of the colon.[75]
Other evidence about the benefit of sigmoidoscopy screening (at which time both polyps and early cancer would be removed) suggests that the impact of endoscopic screening, at least on the left side of the colon, is substantial and prolonged. In an RCT, 170,000 persons were randomly assigned to one-time sigmoidoscopy versus usual care. At sigmoidoscopy, polyps were removed and cancer was detected and referred for treatment. Based on sigmoidoscopy findings, persons were considered to have low risk if they had normal exams or only one or two small (<1 cm) tubular adenomas; such persons were not referred either for colonoscopy workup, or for colonoscopic surveillance. In a follow-up of 10 years, the left-sided CRC incidence in the low-risk group (about 95% of attendees were low risk) was 0.02% to 0.04% per year—a very low risk of CRC compared with average risk. The cause of reduced risk—whether due to detection and removal of large polyps or small ones, or selection of individuals at lower risk—is yet unclear.[76] The natural history of large polyps is not well known, but some evidence suggests that such lesions become clinical CRC at a rate of approximately 1% per year.[77] As a result of the strong data about the impact of endoscopy on the left colon, evidence from multiple studies has raised questions about the ability of endoscopy to reduce CRC mortality in the right colon.[78,79,80] Thus, it is unclear what the overall impact of endoscopy (e.g., colonoscopy screening) is, and whether there may be a large difference in impact on the left side of the colon compared with the right side.[78]
Other studies suggest that the polyps with the greatest potential to progress to CRC are larger polyps (i.e., >1.0 cm), which include most of those with villous or high-grade histologic features. Retrospective cohort studies also show the harms associated with polypectomy, including bleeding.[81,82]
Dietary fat and meat intake
Colon cancer rates are high in populations with high total fat intakes and are lower in those consuming less fat.[83] On average, fat comprises 40% to 45% of total caloric intake in high-incidence Western countries; in low-risk populations, fat accounts for only 10% of dietary calories.[84] In laboratory studies, a high-fat intake increases the incidence of induced colon tumors in experimental animals.[85,86] Several case-control studies have explored the association of colon cancer risk with meat or fat consumption as well as protein and energy intake.[10,87] Although positive associations with meat consumption or with fat intake have been found frequently, the results have not always achieved statistical significance.[88] A number of prospective cohort studies have been conducted in the United States and abroad. In Japan, an increased risk of colon cancer with increased frequency of meat consumption was observed in the group with infrequent vegetable consumption among a group of 265,000 men and women.[89] In Norway, an increased risk for processed meat only was found,[90] a finding that was confirmed in the Netherlands.[91] A clearly defined gradient in the risk for frequency of meat and poultry consumption was not observed in a population of Seventh Day Adventists that included a large proportion of vegetarians.[92] A prospective study among female nurses showed an increased risk of colon cancer associated with red meat consumption (beef, pork, lamb, and processed meat) and also with the intake of saturated and monounsaturated fat, predominantly derived from animals.[93] In two other large prospective studies, the American Cancer Society's CPS II and the Iowa Women's Health Study, no increase in the risk of meat or fat consumption was seen.[94,95] In a prospective cohort study of a low-risk population of non-Hispanic white members of the Adventist Health Study, a positive association between meat (both red and white) intake and colon cancer was observed (RR for ≥1 time per week vs. no meat intake = 1.85, 95% CI, 1.19–2.87, P for trend = .01).[96] It has been hypothesized that the heterocyclic amines (HCAs) formed when meat and fish are cooked at high temperatures may contribute to the increased risk of CRCs associated with meat consumption that has been observed in epidemiologic studies. A population-based case-control study in Sweden, however, found no evidence of increased risk associated with total HCA intake; for colon cancer the RR was 0.6 (95% CI, 0.4–1.0), and for rectal cancer it was 0.7 (95% CI, 0.4–1.1).[97,98]
A randomized controlled dietary modification study was undertaken among 48,835 postmenopausal women aged 50 to 79 years who were also enrolled in the WHI. The intervention promoted a goal of reducing total fat intake by 20%, while increasing daily intake of vegetables, fruits, and grains. The intervention group accomplished a reduction of fat intake of approximately 10% more than the 8.1 years of follow-up. There was no evidence of reduction in invasive CRCs between the intervention and comparison groups with a HR of 1.08 (95% CI, 0.90–1.29).[99] Likewise, there was no benefit of the low-fat diet on all-cancer mortality, overall mortality, or cardiovascular disease.[100]
Explanations for the conflicting results regarding whether dietary fat or meat intake affects the risk of CRC [91] include:
In addition, some epidemiological studies have reported lower incidence rates of colon cancer in populations with high intakes of both fat and fiber, compared with populations with high levels of fat but low levels of fiber consumption.[103] Although far from clear-cut, the available evidence suggests CRC risk is possibly associated with some interaction of dietary fat, protein, and caloric intake.
Six case-control studies and two cohort studies have explored potential dietary risk factors for colorectal adenomas.[20,104] Three of the eight studies found that higher fat consumption was associated with increased risk. High fat intake has been found to increase the risk of adenoma recurrence following polypectomy.[105] In a multicenter randomized controlled trial (RCT), a diet low in fat (20% of total calories) and high in fiber, fruits, and vegetables did not reduce the risk of recurrence of colorectal adenomas.[106]
Thus, the evidence is inadequate to determine whether reducing dietary fat and meat would reduce CRC incidence.
Bile acids
A central effect of bile acids in the etiology and pathogenesis of CRC has been claimed.[107] An increased bile acid concentration in the intestinal tract accompanies a high-fat diet because bile acids are released from the gallbladder after fat ingestion. The concentration of bile acids in the colon is heavily influenced by the amount and type of fat in the diet.[108] The potential mechanism of action of bile salts in colorectal carcinogenesis is unknown, although it has been suggested that it is mediated by diacylglycerol.[109] The conversion of dietary phospholipids to diacylglycerol by intestinal bacteria is enhanced by a high-fat diet. It is proposed that diacylglycerol enters the cell directly, stimulating protein kinase C, which is involved in intracellular signal transduction. There is no high quality evidence from either observational studies or RCTs to substantiate this claim.
Dietary fiber, vegetables, and fruit
The evidence on whether dietary fiber exerts a protective role in reducing the incidence of CRC is mixed. Most animal and epidemiologic studies show a protective effect of dietary fiber on colon carcinogenesis.[51] The term fiber is used to describe a complex mixture of compounds, including insoluble fiber (typified by wheat bran and cellulose) and soluble fiber (usually dried beans). Ingestion of fiber could modify carcinogenesis in the large bowel by a number of potential mechanisms.[110,111,112] These mechanisms include binding to bile acids, increasing fecal water and possibly diluting carcinogens, and decreasing transit time (not an obvious factor). Fiber may act as a substrate for bacterial fermentation with a resultant increase in bacterial mass and the production of short-chain fatty acids, typified by butyrate.[112] Butyrate has been shown to have anticarcinogenic effects in vitro and is regarded as an important fuel for the colonic epithelium.[113,114] A meta-analysis of 13 case-control studies from nine countries concluded that intake of fiber-rich foods is inversely related to cancers of both the colon and rectum.[115] The analysis did not include fiber supplements. The inverse association with fiber was observed in 12 of the 13 studies and was similar in magnitude for left-sided and right-sided colon and rectal cancers, in men and women, and in different age groups. It has been suggested that the inverse association with fiber may be reflective of some other closely associated dietary constituents, such as the anticarcinogens found in vegetables, fruits, legumes, nuts, and grains.[10,115] These substances include phenolic compounds, sulfur-containing compounds, and flavones.[116,117] In a prospective cohort study of a low-risk population, an inverse association was found with legume intake and the risk of CRC (RR for >2 times/week vs. 1 time/week = 0.53 [95% CI, 0.33–0.86; P for trend = .03]).[96]
Other studies have corroborated the effects of dietary fiber. One study used a supplement of 10 g/day of wheat bran, cellulose, and oat bran and found a decreased mutagenic activity of fecal contents in those receiving wheat bran and cellulose supplementation, although no measurable inhibition was observed during oat bran supplementation.[8] Fecal-total and secondary bile acid excretion increased during oat fiber supplementation.
Despite the evidence from case-control studies of a protective effect, results from the large prospective Nurses' Health Study found no difference in the risk of CRC between women in the highest quintile group compared with the lowest quintile group with respect to dietary fiber, after adjusting for age, known risk factors, and total energy intake (RR = 0.95; 95% CI, 0.73–1.25).[118]
Many epidemiologic studies have examined the relationship between fruit and vegetable intake and the incidence of colon and/or rectal cancer,[119] with considerable variation in findings. Perhaps the most definitive analysis to date is a prospective study that examined dietary intake data based on food frequency questionnaires from 88,764 women in the Nurses' Health Study and 47,325 men in the Health Professionals Follow-up Study.[120] The study included a total of 1,743,645 person-years of follow-up, 937 cases of colon cancer, and 244 cases of rectal cancer. On the basis of analyses adjusted for numerous covariates, the authors found no association in women or men between overall fruit and vegetable consumption and the risk of colon or rectal cancer. Associations were not observed when the data were examined for subgroups of fruits or vegetables (with the exception of legumes, which were associated with an increased risk of colon cancer in women) or individual fruits or vegetables (with the exception of prunes, which were associated with an increased risk of colon cancer in men). Results did not change when data were examined by vitamin use status, smoking status, or family history of CRC, nor were elevated risks seen when individuals with very low levels of fruit and vegetable consumption were compared with those having the highest levels. For women and men combined, the covariate-adjusted RR of colon cancer associated with one additional serving of fruits and vegetables per day was 1.02 (95% CI, 0.98–1.05); the comparable RR for rectal cancer was 1.02 (95% CI, 0.95–1.09).
In a population-based prospective cohort study of 61,463 women in Sweden, individuals who consumed very low amounts of fruits and vegetables (<1.5 servings of fruit and vegetables/day) had a RR for developing CRC of 1.65 (95% CI, 1.23–2.2; P trend = .001) as compared with those individuals who consumed more than 2.5 servings. There was little evidence, however, of a benefit for higher as compared with moderate consumption (more than vs. fewer than 3.5 servings). Limitations of this study are that dietary intake during the study period was not reassessed over time, and the influence of physical activity could not be accurately determined. In addition, the conclusion about very low amounts of intake of fruits and vegetables is based on a retrospective subdivision of the lowest quartile of consumption, and its strength has not been adjusted for other potential confounding factors.[121]
Six case-control studies and three cohort studies have explored potential dietary risk factors for colorectal adenomas.[20,104,118] Four of the nine found an association of fiber, carbohydrates, and/or vegetables with reduced risk. In one study, cases with moderate or severe dysplasia had a significantly lower intake of cruciferous vegetables than those with mild dysplasia. No significant effect of dietary fiber on colorectal adenoma was found in the large cohort study of U.S. nurses.[118]
High-fiber cereal supplements during a 3-year period did not result in a decrease in adenoma recurrence in a RCT of 1,303 individuals.[122] In a multicenter RCT, a diet low in fat (20% of total calories) and high in fiber (18 g of dietary fiber/1,000 kcal) and fruits and vegetables (3.5 servings per 1,000 kcal) was not associated with a reduction in the risk of recurrence of colorectal adenomas.[106]
In a prospective cohort study of 35,215 Iowa women, an inverse association between the risk of colon cancer and vitamin E intake was found; the RR for the highest compared with the lowest quartile was 0.3 (95% CI, 0.19–0.54).[123] The Women's Health Study, however, showed no relationship between CRC in women and the use of 600 IU of vitamin E every other day.[124] In a meta-analysis of 14 randomized trials of supplemental antioxidant vitamins encompassing 170,025 individuals, no evidence of prevention of colorectal adenomas or cancer or other gastrointestinal tumors was found.[125] A systematic review of published observational studies that provide sufficient data to calculate the dose-response relationship of serum 25-hydroxyvitamin D or oral intake of vitamin D with the risk of CRC was conducted. The results suggested that a daily intake of 1,000 IU of vitamin D—half the safe upper limit for intake established by the National Academy of Sciences—and a concentration of serum 25-hydroxyvitamin D of 33 ng/mL were each associated with a 50% lower risk of CRC.[126] In a population-based case-control study, an inverse relationship between vitamin D intake and risk of CRC was found.[127]
A prospective cohort study observed that higher energy-adjusted folate intake in the form of multivitamins containing folic acid was related to a lower risk for colon cancer (RR = 0.69; 95% CI, 0.52–0.93) for intake of more than 400 µg/day compared with intake of 200 µg/day or less after controlling for age, family history of CRC, ASA use, smoking, body mass, physical activity, and intakes of red meat, alcohol, methionine, and fiber.[128] In a double-blind, placebo-controlled, two-factor, phase III randomized clinical trial (ASA/Folate Polyp Prevention Study) involving 1,021 men and women with a recent history of colorectal adenoma, folic acid (1 mg/day) was associated with higher risks of developing at least one advanced adenoma (11.6% for folic acid [n = 35]); 6.9% for placebo [n = 21]; unadjusted RR = 1.67; 95% CI, 1.00–2.80; P = .05). Folic acid ingestion was associated with higher risks of having three or more adenomas and of non-CRCs. There was no effect modification by sex, age, smoking, alcohol use, BMI, baseline plasma folate, or ASA use. There was no apparent effect on overall adenoma incidence (44.1% for folic acid [n = 221]); 42.4% for placebo [n = 206]; unadjusted use ratio 1.04; 95% CI, 0.9–1.20; P = .58).[129]
It has been hypothesized that orally ingested calcium lowers colon cancer risk by binding bile acids and fatty acids, thereby reducing exposure to toxic intraluminal compounds.[130] Indirect effects on bile acid metabolism and a direct effect on colonic epithelial cells are also possible.
Several [131,132,133,134] but not all [104,135] epidemiologic studies have observed an inverse relationship between calcium intake and cancer risk. Interpretation of these studies can be quite complex. In Utah, an inverse relationship between colon cancer and calcium was observed in a study that compared members of the Church of Jesus Christ of Latter-Day Saints (Mormons) and Seventh Day Adventists with a group from the U.S. population at large. Both study groups have higher calcium intakes, mainly milk and dairy products, than the national average. Unlike the Seventh Day Adventists, however, the Mormon group had a consumption of meats and fat similar to that of the general population.
Experimental studies in rodents [136] and some but not all human studies [137,138,139,140] have described a decrease in colonic epithelial cell proliferation after the administration of calcium citrate. Human studies using the labeling index are dependent on a complex methodology.[141] A randomized placebo-controlled trial tested the effect of calcium supplementation (3 g calcium carbonate daily [1,200 mg elemental calcium]) on the risk of recurrent adenoma.[142] The primary endpoint was the proportion of patients (72% of whom were male) in whom at least one adenoma was detected following a first and/or second follow-up endoscopy. A modest decrease in risk was found for both developing at least one recurrent adenoma (adjusted risk ratio [ARR] = 0.81; 95% CI, 0.67–0.99) and in the average number of adenomas (ARR = 0.76; 95% CI, 0.60–0.96). The investigators found the effect of calcium was similar across age, sex, and baseline dietary intake categories of calcium, fat, or fiber. The study was limited to individuals with a recent history of colorectal adenomas and could not determine the effect of calcium on risk of the first adenoma, nor was it large enough or of sufficient duration to examine the risk of invasive CRC. After calcium supplementation is stopped, the lower risk may persist up to 5 years.[143] The results of other ongoing adenoma recurrence studies are awaited with interest. It is important to note that the dose of calcium salt administered may be important; the usual daily doses in trials have ranged from 1,250 to 2,000 mg of calcium.
In a randomized, double-blind, placebo-controlled trial involving 36,282 postmenopausal women, the administration of 500 mg of elemental calcium and 200 IU of vitamin D3 twice daily for an average of 7.0 years was not associated with a reduction in invasive CRC (HR = 1.08; 95% CI, 0.86–1.34; P = .051).[144] The relatively short duration of follow-up, considering the latency period of CRC of 10 to 15 years and suboptimal doses of calcium and vitamin D, may account for the negative effects of this trial, though other factors may also be responsible.[145]
Use of statins
Overall, evidence indicates that statin use neither increases nor decreases the incidence or mortality of CRC. Although some case-control studies have shown a reduction in risk, neither a large cohort study [146] nor a meta-analysis of four RCTs [147] found any effect of statin use.
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Description of the Evidence
Revised text to state that four reports in 2007, 2010, 2011, and 2012 have analyzed long-term follow-up of randomized controlled trials of daily aspirin versus the control (cited Algra et al. as reference 64).
Added text to state that six randomized controlled trials were included in a meta-analysis in which patients were randomly assigned to receive either aspirin or placebo and that mean scheduled duration of trial treatment was 4 years or more; allocation to aspirin in the randomized controlled trials reduced the 20-year risk of death due to colorectal and esophageal cancers.
Added text about a large cohort study that found an association between recent daily aspirin use and lower cancer mortality in the gastrointestinal tract, liver, and bladder among 100,139 analysis-eligible participant from the Cancer Prevention Study II Nutrition Cohort (cited Jacobs et al. as reference 65).
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Thursday, May 3, 2012
Design Leadership in Food Retail
In The Duncan Anderson Design Department Gallery at California State University, Long Beach
Deborah talks about emerging retail food trends and how she and her company design to engage retail consumer experiences. She also talks about the career path she has taken showing her projects and talking about the DLE design process.
Before launching her own firm she established herself in retail as Vice President of Store Design and Construction for Bristol Farms Markets and Wherehouse Entertainment where she was responsible for all aspects of store design & construction from initial strategic planning & design to final construction. With over 20 years in retail design she has overseen all aspects of project development – from strategic planning, through store construction and visual display.
D L English Design was founded in 1996 as an innovative retail design firm with a focus on research-based design and implementation. Experts at niche market design, they create a wide range of store types, from ethnic to natural food communities. They are known for discovering next-level design solutions that are fresh and authentic. Searching the world for inspiration, they use that inspiration to create locally-tailored community stores.
They specialize in food retail and specialty retail; and their passion is in creating intuitive, authentic spaces that embed themselves in the psyche of the shopper through retail branding & design, architectural interiors, and environmental graphics.
Major clients include Whole Foods Markets, Bristol Farms, Schnucks, Trader Joes, and TransWorld Entertainment (FYE stores, and other brands). Key services include Shopper Marketing Solutions, Brand Development, Space Planning & Programming, Lighting Design, Architectural Interior Design, Decor Design, Graphics & Signage, Bidding & Fabrication Coordination.

subset: commoncrawl


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'American Idol' Season 11 Hollywood Week 1 Recap: Symone Black Falls, Jane Carrey Leaves
The Hollywood rounds of 'American Idol' have begun, and a whopping 68 contestants were sent home on the first day. The judges sifted through tons of talent, dashing dreams, breaking hearts and catering to possible future stars. It's a hard shill being an 'Idol' judge, especially when you watch contestant Symone Black fall off the stage right in front of your face.
Here's your PopCrush recap, detailing who did and said what, and who's moving on. Several singers did not have their fates revealed, like David Leathers Jr. and Lauren Mink. That should come tomorrow.
Johnny Keyser: His silky version of 'Dreamin" by Amos Lee warmed the soul so he's sticking around.
Heejun Han: He made J. Lo cry when he revisited 'How Am I Supposed to Live Without You' by Michael Bolton. He's a "yes."
Elise Testone: Her name looks like "testosterone" and she infuses her songs with smoky, husky, somewhat masculine soul.
Baylie Brown: She's countrified and also headed to another round.
Hallie Day: Hallie is another gal with a major voice who knocked '(You Make Me Feel Like) A Natural Woman' out of the park.
Jen Hirsch: She took us up to the peaks with her rendition of 'Up to the Mountain.' Such a pretty tone. Don't stop, girl!
Lauren Gray: She tackled Adele's 'One and Only.' Ballsy, yes, but the judges seem interested in hearing more.
Phillip Phillips: Again, he has the best name ever. He bluesed it up (or down) with 'Papa's Got a Brand New Bag.'
Reed Grimm: He was scatastic and likely watched Casey Abrams last season. He's better, though, and sang about golden tickets, literally. He sang a song from 'Willy Wonka and the Chocolate Factory.'
Travis Orlando: The Bruno Mars lookalike made it one round further this year, but didn't advance to the next phase. Bummer.
Ramiro Garcia: He was born without ears, but had all heart. Sadly, he was sent home.
Jenni Schick: Another early audition fave didn't get another chance.
Adam Brock: This bearded father said he has a large black woman trapped inside of his body. He sang 'Walkin' in Memphis' with loads and loads of soul. We'll see him again.
Jane Carrey: Jim's daughter rocked 'Lookin' Out My Back Door' by Creedence Clearwater Revival. It wasn't good enough to get another pass. No nepotism there.
David Leathers: How does a dude do diva? He soared with 'Because You Love Me' by Celine Dion and Steven Tyler said he has ties older than Leathers. He does things differently, this kid.
Shannon Magrane: She sang 'Fallin" by Alicia Keys just beautifully.
Jessica Phillips: She cares for her boyfriend who had a stroke. She struck a nerve with 'All the Man That I Need,' a Whitney Houston barnburner.
Erika Van Pelt: This mobile DJ has more soul than a church choir. She rocked Pink's 'Glitter in the Air.' More please!
Creighton Fraker: This street artist is moving on too, after he covered Queen's 'Somebody to Love.'
Aaron Marcellus: The high notes were easily conquered by this music teacher.
Lauren Mink: She sang 'Alone' by Heart, but this '80s power ballad was not the right song for her, since she changed keys mid-song. Ouch.
Jeremy Rosado: He sang Luther Vandross' song 'Superstar' and it was infectious. He works at the front desk of an infectious disease doctor's office, too.
Symone Black: While she turned in a lovely rendition of '(Sittin' on) The Dock of the Bay' by Otis Redding, she had a scare when she fell off the stage as she stepped forward to address the judges. The ep ended there and we find out how the teen is doing tomorrow.


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Local governments and police on Wednesday attacked a sweeping proposal to change Maryland's speed camera law.
During the first hearing on whether to revamp a law that has been lucrative for local governments but also has sparked concerns about fairness, speed camera proponents defended what has been called a "bounty system" of paying contractors based on the number of tickets issued to drivers.
Program supporters also rejected as unfeasible a proposal to require precise time-stamped photos and painted lines on roadways that would more easily allow motorists to challenge the $40 tickets in court.
"Our roads would look like zebras," Prince George's County Police Maj. Robert Liberati told a Senate committee in Annapolis, which also heard arguments that the cameras improve public safety.
Several lawmakers are pushing legislation to either rework or repeal the state's 2009 speed camera law after The Baltimore Sun reported that several Baltimore cameras issued tickets to motorists in error. The Sun also showed that several Maryland jurisdictions do not provide the necessary information to challenge tickets.
Since this summer, Baltimore has audited its program, issued refunds to motorists and hired a new vendor to operate new, more sophisticated cameras. Mayor Stephanie Rawlings-Blake set a goal to have "a zero-error program." City cameras have generated $48 million in fines since 2009.
Sen. James Brochin, a Baltimore County Democrat who has proposed a multi-part plan to overhaul the state law, called the city's program an "absolute sham" that was tantamount to a "commuter tax" on people driving into the city.
Brochin's proposal calls for more clearly outlawing per-ticket payments to speed camera contractors, giving motorists more evidence of their speeding infractions and imposing greater limits on when and where cameras can be placed.
In his pitch to fellow lawmakers, Brochin offered photos of camera placed outside the Broadcasting Institute of Maryland on Harford Road as evidence that local governments can misuse the current law by broadly interpreting what counts as a school zone. His bill would restrict the cameras to within 500 feet of an elementary or secondary school.
Lawmakers also heard testimony on a bill to repeal the speed camera law altogether. "We launched the program too quickly," said Sen. E.J. Pipkin, an Eastern Shore Republican. "It turned out to be an embarrassment in Baltimore City."
Brochin said he also would prefer repeal, but was a "political pragmatist." He said his proposal was "the best fix that I could come up with."
While several people with objections to speed camera programs urged lawmakers to adopt stricter rules and greater transparency, Brochin's proposal drew criticism from several other jurisdictions with speed camera programs. The Maryland Association of Counties called Brochin's proposal "needless and potentially detrimental."
Montgomery County Police Capt. Tom Didone oversees that jurisdiction's speed camera program, the state's oldest. He said proposals to overhaul the law would be "ineffective, impractical, unnecessarily expensive and do not address the primary concern for these programs."
Didone said problems with some camera programs could be attributed to human error.
In a letter to the Senate Judicial Proceedings Committee, the Maryland Department of Transportation said that Brochin's proposal would force the state to "implement an inferior" program to the laser-based system that catches speeders in highway work zones.
Prince George's County Executive Rushern Baker wrote that the time-stamp requirement could possibly put that jurisdiction's 72 mobile cameras off-line.
Other proposals to change the state's speed camera law will receive public hearings over the next several weeks.


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Atlanta 1 Whitecaps 0: Quiet storm capsizes Caps' win streak
If a tree falls in the forest, or the Vancouver Whitecaps lose a game and there's no one there to see it, did it really happen?
B.C. Place wasn't empty for Wednesday night's 1-0 to Atlanta United, but the announced crowd of 16,138 left the confines of the Dome feeling cavernous and quiet. Even the 35th minute walkout by the Vancouver Southsiders and Curva Collective lacked much impact, with the stadium already feeling half empty.
It was the smallest crowd at B.C. Place since June 19, 2013, when the Caps had 16,130 on hand to watch a 3-1 win over Chivas USA in another Wednesday matchup. Tonight's game was the third-lowest since the Caps have been in B.C. Place in MLS play, with the lowest coming on April 18, 2012, when 15,382 took in a 3-1 loss to Kansas City — the Caps' host on Saturday.
Josef Martinez scored for Atlanta (6-3-2), who have now won five straight games — all by shutout, a new MLS record. Vancouver (3-6-3) had a two-game win streak snapped, their first loss since April 20.
Here's what we learned:
Vancouver Whitecaps vs. Sporting Kansas City
5:30 p.m. Children's Mercy Park, TV: TSN Radio: TSN1040
Max Effort
The best player for the Whitecaps, by a wide margin, was goalkeeper Max Crepeau. He had his second-straight five-save performance, including a three-stop sequence with acrobatic, point-blank saves on Hector Villalba, Eric Remedi and Pity Martinez.
He also had another save on Josef Martinez later in the half to keep Vancouver in the game. He couldn't do anything on Josef Martinez's penalty shot — the MLS-high seventh they've surrendered — despite guessing right and diving to the left, with the shot just squeaking between his hand and the post.
"That's why we have Max. That's why he plays for the club," said Caps coach Marc Dos Santos. "When those saves happened, I said it was an extra (boost) and we're going to score. And it didn't happen."
His Atlanta counterpart, Brad Guzan, now extended his shutout streak to 456 minutes — the longest active shutout streak in MLS.
Penalty Puzzle
When Lass Bangoura took down Pity Martinez in the box midway through the first half, it led to the seventh penalty kick conceded by Vancouver this season. Josef Martinez cooly slotted it home past Crepeau for the game's only goal.
For the second straight season, the Caps are leading the league in penalty kick goals conceded, after giving up nine in 2018. You could forgive the team for feeling cursed, with the amount of turnover in personnel from top to bottom giving way to the same results.
Dos Santos has been baffled by his team's propensity to give up PKs, the last three all coming as a result of clumsy challenges where plays were, as he repeatedly stated, "under control."
A failed clearance led to Wednesday's foul, but there was little need for Bangoura's defensive blunder, as Pity Martinez was bracketed by Ali Adnan on the left, between the Five Stripes player and goal.
"The penalty shot, again, is very clumsy. It's a play that's under control, but Ali is there with him. It's frustrating to lose like that. That's frustrating. I don't have a clue how I'm going to deal with that," said Dos Santos. "It's incredible. It's a new (problem) for me. It's way too many. I think that in the ones we've given away, many are clumsy. I'm going to think about how to address it."
Brek-Fast Meal
He was supposed to be the weak link, a walking meme for Caps fans to share, but Brek Shea walked out of B.C. Place Wednesday night not only beating his former club, but looking little like the player he was in Vancouver.
He was defensively sound at left back, handling any crosses or penetration attempts from Lucas Venuto, and finished the game as Atlanta's top-rated player, according to whoscored.com.
Shea also put a pinpoint cross on the head of Josef Martinez in the 68th minute, whose header forced Crepeau into a diving save.
While the rest of his team was greeted with the usual shouts of "wanker" from the Caps supporters at the start of the game, Shea, who signed with Atlanta in the off-season, was greeted with a slightly sarcastic cheer from the crowd.
Golden Boot Heating Up
Josef Martinez, last year's Golden Boot winner with 31 goals, had just one goal through his team's first five games. He's now scored four in his last six, with two assists.
The Venezuelan striker started up top Saturday and converted a quality penalty kick to put the visitors up 1-0 in the 29th minute. He only had a team-low 15 touches in the first half, although the 5-foot-7 striker was just inches short on connecting on a pair of headers and made a few probing runs that tested the Caps defence.
"It's like music, you know: small pass, and then suddenly you accelerate, and you feel the danger," Atlanta coach Frank de Boer said of his forward earlier this week.
"Everybody feels in the crowd or me, myself, will see, 'Oh there's something happening.'"
Stats Book
The stats were once again weighted against the Caps, as the home side padded its lead atop MLS in shots allowed — coming into Wednesday at 17.4 per game — after being outshot 17-7, including 6-2 on target.
The Whitecaps' passing was solid in possession in their own third, contributing to a decent 80 per cent overall, but final third passing accuracy was again left wanting, ending with 60 per cent.
The Caps did win the possession battle with 54.3 per cent of the ball, and won the duels battle 51-41, but the only stat that really mattered was the 1-0 final scoreline.
Dos Santos said this week he was happy with the number of shots conceded — even coming off a 27-attempt performance versus Portland — and looked at the stats on a by-game basis, depending on what they were attempting to do tactically.
"We look at the stats, we look at all of that. But we also look at the game," he said this week. "We look at the stats, and then look at them based on what we wanted to do in the game. One of the examples is, if you look at the stats, we're a team that allows more crosses in. You can look at it, and say 'Oh, s**t, they allow so many crosses' but we look at it and say 'Great! They aren't able to penetrate us inside, they have to go around and cross, where I feel we defend them very well.'
"We look at the stats, we look at the model of play, we look at what we wanted to reach against a certain opponent, and we say 'this is good that this happened,' or 'this is bad that this happened.'"


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Studio on course to be the most "up-to-date, highly equipped studio in the country", according to COO Maria Walker [pictured].
Three months after property magnate Sunny Vohra was revealed as Twickenham Film Studios' mystery buyer, the studio has attracted clients and ordered enough equipment to make it the most "up-to-date, highly equipped studio in the country," according to Chief Operating Officer Maria Walker.
Walker, who headed the campaign to save Twickenham from being closed in June, announced last night at the Rembrandt Hotel in London that Twickenham had acquired three new mixing consoles - including two DFC Geminis - for each of the studio's theatres.
"We are doing a lot," Walker told Screen. "We're getting the word out that we are the best studio post-production facility in the country."
Twickenham is looking to install $1.6m in equipment by spring. The studio has already bought 3D projectors and Dolby Atmos surround sound for one of its theatres. There are also plans to build three television mixing rooms and one grading suite, as well as refurbish the changing, hair and make-up rooms.
Two of the studio's three theatres are currently being used, Walker said, although she could not say who was renting them. She added that all three stages will be in use next week and that the studio recently finished an IMAX film.
The Twickenham staff is also expanding, which Vohra said was one of his goals. Two new engineers, one sound team member, the first-ever sales manager and the first-ever public relations representative have been added.
Walker could not say how much Vohra had invested in Twickenham, but said that considering the "massive expenditure on the infrastructure of the building, refurbishing and upgrading, it's a lot of money."
Twickenham hopes to remind the international and local film industry that it's up and running by improving its social media presence and attending the forthcoming AFM, among other events.
Twickenham is renowned for the production of recent award-winning films such as The Iron Lady, My Week With Marilyn and Elizabeth: The Golden Age.


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Kate Mackie
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Emeritus Sr. Lecturer
Professor Mackie has had 14 years in positions of increasing responsibility in marketing, new business development and management in major corporations, including over 11 years with The Pillsbury Company. Background includes marketing, market research, strategic and tactical planning, budget development, capital planning, staff management and development, business start-up, advertising agency interaction and 5 years of international business management. Five years experience related to Total Quality Management, including research and evaluation, community service with the Austin Quality Council, seminar development and leadership, client consultation, and facilitation. Currently teaching at The University of Texas at Austin, College and Graduate School of Business. Education includes a Ph.D. in Educational Psychology, a master's degree in International Management, and a bachelor's degree in Secondary Education. Professor Mackie is fluent in Spanish.
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Longtime Milwaukee Brewers groundskeeper dies
Man collapsed in bullpen during game Sunday
MILWAUKEE — A longtime groundskeeper for the Milwaukee Brewers collapsed during a game and died.
The team says 51-year-old Jeff Adcock collapsed in the home bullpen during the game against the Arizona Diamondbacks Sunday.
The game was delayed at the top of the second while medical personnel tried to revive him, but he died at a hospital. Adcock was grounds crew lead and had worked there for 33 years.
The Brewers won 2-1.
The Milwaukee County medical examiner noted Adcock likely died of natural causes but isstill investigating the cause.
In a statement, Bob Quinn, the team's executive vice president for finance and administration, said Adcock developed many friendships with the staff, and he will be missed.
Last fall, head groundskeeper Gary Vanden Berg died after a long battle with cancer.


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|Chapter 40. libpq
The copy command in Postgres has options to read from or write to the network connection used by libpq. Therefore, functions are necessary to access this network connection directly so applications may take full advantage of this capability.
PQgetline Reads a newline-terminated line of characters (transmitted by the backend server) into a buffer string of size length. Like fgets(3), this routine copies up to length-1 characters into string. It is like gets(3), however, in that it converts the terminating newline into a null character. PQgetline returns EOF at EOF, 0 if the entire line has been read, and 1 if the buffer is full but the terminating newline has not yet been read. Notice that the application must check to see if a new line consists of the single character ".", which indicates that the backend server has finished sending the results of the copy command. Therefore, if the application ever expects to receive lines that are more than length-1 characters long, the application must be sure to check the return value of PQgetline very carefully. The code in ../src/bin/psql/psql.c contains routines that correctly handle the copy protocol.
int PQgetline(PGconn *conn, char *string, int length)
PQputline Sends a null-terminated string to the backend server. The application must explicitly send the single character "." to indicate to the backend that it has finished sending its data.
void PQputline(PGconn *conn, char *string);
PQendcopy Syncs with the backend. This function waits until the backend has finished the copy. It should either be issued when the last string has been sent to the backend using PQputline or when the last string has been received from the backend using PGgetline. It must be issued or the backend may get "out of sync" with the frontend. Upon return from this function, the backend is ready to receive the next query. The return value is 0 on successful completion, nonzero otherwise.
int PQendcopy(PGconn *conn);
PQexec(conn, "create table foo (a int4, b char16, d float8)"); PQexec(conn, "copy foo from stdin"); PQputline(conn, "3<TAB>hello world<TAB>4.5\n"); PQputline(conn,"4<TAB>goodbye world<TAB>7.11\n"); ... PQputline(conn,".\n"); PQendcopy(conn);
|Asynchronous Notification
|libpq Tracing Functions


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I had a meeting last week with some people involved in adult education. As a writer who counts teaching creative writing as one of her jobs, it's an area that I hover at the fringes of. On the one hand, yes, I teach adults (some of the time) – they are evening classes; they are for self-improvement; they are usually people who come not just in search of facts and figures but how to apply what they already know to what they're trying to do next and how to learn in this new field. On the other hand, they are not practical in the sense of providing one with a certificate that can be used to go on and do something else with; they are not things you pass or fail.
I'm on the fringes of 'ordinary' education too. I'm not an English teacher. I sometimes go into English classes or school libraries, but I'm not there to teach the syllabus and get students passing their exams. I teach on specialist programmes, things that complement the 'normal' education people get in school. So it maybe wasn't too surprising that I found myself surprised by the way 'adult education' was conceptualised as something opposed to 'ordinary education', as though children will simply absorb whatever you say without questioning its purpose while adults need to see the relevance of something to their own experience. When we talked about the kinds of activities that might be suitable to adult ed, I found myself drawing on activities I use at a summer course I teach to/facilitate for teenagers. It seems so bizarre to me that lines are drawn between the adult ed student and the regular student, the grown-up and the adolescent. When you teach the stuff that's not on the syllabus, in environments where learners are more often than not there because they want to be, you see the similarities much more than the differences.
The same week, I read yet another book about gifted children, When Gifted Kids Don't Have All The Answers. One of the specialist programmes I teach on is aimed at gifted kids and teens, and it's an area that fascinates me, so I try to keep up with the books and guides and research as much as I can. There's one part that stays with me – a comment about how we so often tell kids it's okay 'as long as they did their best' or we tell them 'just do your best'. At everything. And it asks us, how many adults do we know that do their best at everything they do?
We live in an era of retraining and career-shifting, a time when adults are often continuing education formally or informally, trying to improve themselves or change themselves. We see what works for adult learners and we develop new ways of teaching and facilitating accordingly. I just wonder how much of that we can apply to younger learners, rather than assuming they are somehow 'built' to learn or that there are skills necessary for learning that we want young people to have but don't have ourselves and somehow manage to get by. There are things that younger learners don't know, haven't experienced, have trouble with, sure – but they're not entirely different creatures.
For any of the rest of you, readers or contributors, what do you think of the differences between learning as an adult and learning at a 'standard' age? Do we expect something different from our experiences learning as an adult – or do we respond to the different way we're taught?


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Fourth SineQuaNet workshop, to be held in Frascati, Italy
On 28 March ESA's SME Unit will hold a SineQuaNet workshop in Frascati, Italy with representatives of industry and other space actors to address important issues for small and medium sized enterprises (SMEs) operating in or wanting to enter the space sector.
The workshop is the last in a series of four designed to reinforce mutual understanding of the means and methods by which the foreseen SineQuaNet (Space Intelligence, Engineering and Quality Network) could effectively build and deliver relevant support to SMEs. More than 100 professionals from European enterprises, research institutes and space industry support organisations attended each of the previous three workshops, held respectively in The Netherlands, the UK and Germany.
The SineQuaNet project was launched in November 2005 by ESA, with support from the European Commission, to elaborate a genuine structuring mechanism focused on technical and engineering support. It is targeted at European and Canadian SMEs already operating in, or wanting to enter, the space sector.
The network aims to organise, structure and improve SME's access to technical facilities, expert support and training services. Although these are already available within the space sector from large organisations, systems integrators, and research institutes, a wide range of SMEs remain impeded from access to resources of this kind.
A dedicated expert database of available resources will be setup through which all entities - whether SMEs, large groups, universities or laboratories - can offer the services of their own experts, or the use of technical facilities and laboratories, on a fair compensation basis. In this way, the service providers will benefit from a more profitable use of their experts as well as a better return on investment in their facilities.
Sinequanet is now in its first phase of defining and setting up its activities. These are:
- establishing the needs of SMEs for hands-on expertise, training and access to facilities for testing and calibration of new technologies and systems
- testing the Sinequanet concept by providing actual support to two SMEs
- creating a database containing sources of expertise and suppliers of facilities and services
- holding a series of workshop meetings, of which the Frascati meeting 28 March is one, at various locations throughout Europe, where SMEs and other industrial partners can meet to exchange views and refine the objectives of SineQuaNet
- creating a dedicated website as a communication and information tool for SMEs within the space sector. This new website was set-up last year and launched 7 December 2006, at http://www.esa.int/sme.
The workshop on 28 March will take place at ESRIN, ESA Centre for Earth Observation in Frascati, Italy. Registration by companies wishing to participate must be done at the dedicated SineQuaNet Workshop Programme website (http://www.isd2006.com/WP5/), where also more information is provided. Early registration is advised as the number of attendees is limited.
The SineQuaNet (Space INtelligence, Engineering & QUAlity NETwork) project is run by ESA's SME Unit, with support from the European Commission's 6th Framework Programme, Economic & Technology Intelligence.


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Just read a news on reuters about aafia siddiqui, 5 feet week lady, allegedly linked with al-qaida and serving 86 years imprisonment for snatching a gun from 3 strong marines in prison and in the process getting herself shot without having any finger prints on the gun (according to trial reports and testimony of fbi agent in the court). First USA media was saying Ammar Al-Baluchi is Aafia's husband and now they are saying Majid Khan is her husband? We also need an open trial in Pakistan to see who is her husband? It seems they are not consistent in their 9/11 lies and deception.
Even the bogus wikipedia entry on her still says Al-baluchi as her husband and many US media sources of that time (though her family denies any of these reports). http://en.wikipedia.org/wiki/Aafia_Siddiqui
Justice, humanity and peace loving people in USA should raise their voice on the issue.
Something relevant to current times, written in Nazi days by Pastor Martin Niemoller :
First they came for the communists,
and I didn't speak out because I wasn't a communist.
Then they came for the trade unionists,
and I didn't speak out because I wasn't a trade unionist.
Then they came for the Jews,
and I didn't speak out because I wasn't a Jew.
Then they came for me
and there was no one left to speak out for me.
Update : Reuters have recognized their mistake and have now edited the story with a note at the end : (In para 12, removes incorrect description of Aafia Siddiqui as Khan's wife; she is not his wife)


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How Big Tech Makes Their Billions
Visualizing the Size of Amazon, the World's Most Valuable Retailer
What's At Risk: An 18-Month View of a Post-COVID World
Vegetarianism: Tapping Into the Meatless Revolution
Tesla is Now the World's Most Valuable Automaker
The Future of Remote Work, According to Startups
What Does 1GB of Mobile Data Cost in Every Country?
10 Types of Innovation: The Art of Discovering a Breakthrough Product
Visualizing the Rise of Digital Payment Adoption
The Racial Wealth Gap in America: Asset Types Held by Race
Golden Bulls: Visualizing the Price of Gold from 1915-2020
All of the World's Money and Markets in One Visualization
How U.S. Consumers are Spending Differently During COVID-19
CBD Oil vs. Hemp Oil: What's the Difference?
The COVID-19 Impact on Advertising Spend
Visualizing the Growth of COVID-19 in the U.S., Organized by State Peak Date
6 Ways Hydrogen and Fuel Cells Can Help Transition to Clean Energy
Visualizing America's Energy Use, in One Giant Chart
The New Energy Era: The Impact of Critical Minerals on National Security
How Oil Prices Went Subzero: Explaining the COVID-19 Oil Crash
How to Avoid Common Mistakes With Mining Stocks (Part 2: Business Plan)
Gold in Nevada: The Real Golden State
Mapped: The Geology of the Moon in Astronomical Detail
How China's Plastics Ban Threw Global Recycling into Disarray
Visualizing the Human Impact on the Ocean Economy
Political Longshots That Caught America by Surprise
Visualizing the True Size of Land Masses from Largest to Smallest
11 Cognitive Biases That Influence Political Outcomes
Mapped: The State of Press Freedom Around the World
The Cost and Composition of America's Nuclear Weapons Arsenal
As unemployment levels rise, we navigate the fallout of COVID-19 as layoffs ripple across the once-thriving startup ecosystem.
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Daily Slice: Sausage Slice from Celebre's, Philadelphia
A different slice profiled each day.
Daily Slice gives a quick snapshot each weekday of a different slice or pie that the folks at the Serious Eats empire have enjoyed lately.
Celebre's has quickly become my new favorite South Philly delivery spot. Caroline wrote about their Pizzaz a while back (supposedly they are the originators) and since then I've been ordering from them on a regular basis. Their sausage comes in awesome thin pork ribbons that crisp up on the edges like pepperoni. The decorative green peppers are also a nice touch.
Celebre's has one of the thinner crusts in the old-school Philadelphia pizzeria world, always with nice color on the bottom and never greasy, soggy, or soupy. The sauce is more spicy than sweet and overall it's just completely different from the homogeneous South Philly style —rumored to stem from the mafia forcing every pizzeria to use the same cheap ingredients back in the day. Their slice is definitely in my South Philly top 5.
Celebre's Pizza
1536 Packer Avenue, Philadelphia, PA 19145-5407 (map) (215) 467-3255; celebrespizza.com
All products linked here have been independently selected by our editors. We may earn a commission on purchases, as described in our affiliate policy.


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We've got a few casting stories for you today. First up, Matthew Macfadyen (The Three Musketeers) has joined the cast of director Joe Wright's (Hanna) adaptation of Anna Karenina. The Daily Mail (via Dark Horizons) reports that Macfadyen replaces Benedict Cumberbatch in the role of Oblonsky in the film version of Leo Tolstoy's classic tragic love story. In addition to Macfadyen, Olivia Williams, Domhnall Gleeson and Andrea Risebourough have joined the cast as well. Keira Knightley, Jude Law, Aaron Johnson and Kelly Macdonald are set to star in the Tom Stoppard-scripted (Shakespeare in Love) flick. Filming is set to begin this fall.
Next up, Patricia Arquette has joined the cast of brother David's directing vehicle Glutton. The psychological thriller stars Abraham Benrubi (ER) as a 1,200 pound bedridden man. Arquette and Kacey Barnfield play the two female leads in the 3D flick. Variety reports that Arquette will play the man's sister, while Barnfield will take on the role of a blind neighbor. Hit the jump for the casting of Adhir Kalyan in the indie film Samaritan as well as a synopsis of the book Anna Karenina.
Rules of Engagement star Adhir Kalyan has joined the cast of the indie drama Samaritan. The film centers on a community college student who stops a girl from committing suicide, only to have her torment the rest of his life. Variety reports that Kalyan will play one of the protagonist's closest friends who becomes concerned with the relationship between the suicide attempt victim and his friend. Trevor Morgan and Thomas Jane also star in the film.
Here's the synopsis for Anna Karenina:
Married to a powerful government minister, Anna Karenina is a beautiful woman who falls deeply in love with a wealthy army officer, the elegant Count Vronsky. Desperate to find truth and meaning in her life, she rashly defies the conventions of Russian society and leaves her husband and son to live with her lover. Condemned and ostracized by her peers and prone to fits of jealousy that alienate Vronsky, Anna finds herself unable to escape an increasingly hopeless situation. Set against this tragic affair is the story of Konstantin Levin, a melancholy landowner whom Tolstoy based largely on himself. While Anna looks for happiness through love, Levin embarks on his own search for spiritual fulfillment through marriage, family, and hard work. Surrounding these two central plot threads are dozens of characters whom Tolstoy seamlessly weaves together, creating a breathtaking tapestry of nineteenth-century Russian society.


text: I was in Costco the other day and they had a HP notebook for $349.00 Not sure of the specs on it, but I played around with it for about 1/2hour and almost tried to convince myself to get it. I might still get it because I take minutes for a non profit agency that meets a few times a month and I am always shlepping that heavy laptop. That's what I want it for, also surfing when I go traveling.


text: All eggs sold in stores are grade A, so the "choice" of grade is a no-brainer. But these days, you'll find plenty of other labels on eggs, intended to make you buy one particular product or another. Because the choices can be dizzying and unclear, it can be difficult to know what is best for your family. To help you sort things out, here are some terms and a little information about what each means—or doesn't mean.


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How can my yard be changed so that it will look new and fresh? What can I do to have a landscape that will be the envy of everyone? To find the answers you seek as well as some helpful landscaping advice, read the tips contained here in this article.
Sketching out what you would like your final landscaping job to look like is beneficial. You'll be able to get a clear idea of the results and the materials needed to achieve those results. You can also easily make changes to the sketch, as opposed to making changes to the actual lawn.
Add soft curves to the edges of your rock beds and flower beds for an instant update. A curved edge looks modern, smooth and beautiful, and can really enhance your design. Cutting a crisp edge is inexpensive, and it will make your landscape look manicured.
Maximize your landscaping work by designing a year-round outdoor space. Select plants that will grow in the fall, spring, summer and winter, as is realistic for your area. You can also pick trees with nice foliage or evergreens which make your yard look alive all year long.
You don't have to pay a designer or landscaper for your projects, regardless of what many people believe. This will cause you to lose a lot of money. However, it might be a good idea to consult with a professional so you can figure out what is wrong and right about your plan.
You get what you pay for. If you always choose the cheapest material, you may not get the quality that you want. If you're new when it comes to landscaping, specialty stores can give you better advice and guarantees, even though they are more pricey.
The tips and ideas in this article should be able to help anyone who wishes to improve their landscaping. Regardless of how much landscaping you intend to do or where you want to start, you should be ready to begin now that you've read this article.
Landscaping Tips That Can Save You Frustration!